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        <title>ENDOCR REV via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'ENDOCR REV' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=ENDOCR+REV&t=ENDOCR+REV&s=Search&f=source]]></link>
        <lastBuildDate>Mon, 15 Mar 2010 14:24:35 +0100</lastBuildDate>
        <item>
            <title>The Melanocortin-4 Receptor: Physiology, Pharmacology, and Pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=3323261&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20190196%26dopt%3DAbstract</link>
            <description>Authors: Tao YX
    The melanocortin-4 receptor (MC4R) was cloned in 1993 by degenerate PCR; however, its function was unknown. Subsequent studies suggest that the MC4R might be involved in regulating energy homeostasis. This hypothesis was confirmed in 1997 by a series of seminal studies in mice. In 1998, human genetic studies demonstrated that mutations in the MC4R gene can cause monogenic obesity. We now know that mutations in the MC4R are the most common monogenic form of obesity, with more than 150 distinct mutations reported thus far. This review will summarize the studies on the MC4R, from its cloning and tissue distribution to its physiological roles in regulating energy homeostasis, cachexia, cardiovascular function, glucose and lipid homeostasis, reproduction and sexual function,...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3323261</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>The Role of Blood Vessels, Endothelial Cells, and Vascular Pericytes in Insulin Secretion and Peripheral Insulin Action.</title>
            <link>http://www.medworm.com/index.php?rid=3288578&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20164242%26dopt%3DAbstract</link>
            <description>Authors: Richards OC, Raines SM, Attie AD
    The pathogenesis of type 2 diabetes is intimately intertwined with the vasculature. Insulin must efficiently enter the bloodstream from pancreatic beta-cells, circulate throughout the body, and efficiently exit the bloodstream to reach target tissues and mediate its effects. Defects in the vasculature of pancreatic islets can lead to diabetic phenotypes. Similarly, insulin resistance is accompanied by defects in the vasculature of skeletal muscle, which ultimately reduce the ability of insulin and nutrients to reach myocytes. An underappreciated participant in these processes is the vascular pericyte. Pericytes, the smooth muscle-like cells lining the outsides of blood vessels throughout the body, have not been directly implicated in insulin se...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288578</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288578</guid>        </item>
        <item>
            <title>The Role of Mitochondria in the Pathogenesis of Type 2 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=3280627&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20156986%26dopt%3DAbstract</link>
            <description>Authors: Patti ME, Corvera S
    The pathophysiology of type 2 diabetes mellitus (DM) is varied and complex. However, the association of DM with obesity and inactivity indicates an important, and potentially pathogenic, link between fuel and energy homeostasis and the emergence of metabolic disease. Given the central role for mitochondria in fuel utilization and energy production, disordered mitochondrial function at the cellular level can impact whole-body metabolic homeostasis. Thus, the hypothesis that defective or insufficient mitochondrial function might play a potentially pathogenic role in mediating risk of type 2 DM has emerged in recent years. Here, we summarize current literature on risk factors for diabetes pathogenesis, on the specific role(s) of mitochondria in tissues involve...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3280627</comments>
            <pubDate>Mon, 15 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Kallikreins on Steroids: Structure, Function, and Hormonal Regulation of Prostate-Specific Antigen and the Extended Kallikrein Locus.</title>
            <link>http://www.medworm.com/index.php?rid=3215046&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103546%26dopt%3DAbstract</link>
            <description>Authors: Lawrence MG, Lai J, Clements JA
    The 15 members of the kallikrein-related serine peptidase (KLK) family have diverse tissue-specific expression profiles and putative proteolytic functions. The kallikrein family is also emerging as a rich source of disease biomarkers with KLK3, commonly known as prostate-specific antigen, being the current serum biomarker for prostate cancer. The kallikrein locus is also notable because it is extraordinarily responsive to steroids and other hormones. Indeed, at least 14 functional hormone response elements have been identified in the kallikrein locus. A more comprehensive understanding of the transcriptional regulation of kallikreins may help the field make more informed hypotheses about the physiological functions of kallikreins and their effec...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215046</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
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            <title>Mortality in Patients with Pituitary Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3198238&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20086217%26dopt%3DAbstract</link>
            <description>Authors: Sherlock M, Ayuk J, Tomlinson JW, Toogood AA, Aragon-Alonso A, Sheppard MC, Bates AS, Stewart PM
    Pituitary disease is associated with increased mortality predominantly due to vascular disease. Control of cortisol secretion and GH hypersecretion (and cardiovascular risk factor reduction) is key in the reduction of mortality in patients with Cushing's disease and acromegaly, retrospectively. For patients with acromegaly, the role of IGF-I is less clear-cut. Confounding pituitary hormone deficiencies such as gonadotropins and particularly ACTH deficiency (with higher doses of hydrocortisone replacement) may have a detrimental effect on outcome in patients with pituitary disease. Pituitary radiotherapy is a further factor that has been associated with increased mortality (particul...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198238</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
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            <title>From Estrogen-Centric to Aging and Oxidative Stress: A Revised Perspective of the Pathogenesis of Osteoporosis.</title>
            <link>http://www.medworm.com/index.php?rid=3149731&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051526%26dopt%3DAbstract</link>
            <description>Authors: Manolagas SC
    Estrogen deficiency has been considered the seminal mechanism of osteoporosis in both women and men, but epidemiological evidence in humans and recent mechanistic studies in rodents indicate that aging and the associated increase in reactive oxygen species (ROS) are the proximal culprits. ROS greatly influence the generation and survival of osteoclasts, osteoblasts, and osteocytes. Moreover, oxidative defense by the FoxO transcription factors is indispensable for skeletal homeostasis at any age. Loss of estrogens or androgens decreases defense against oxidative stress in bone, and this accounts for the increased bone resorption associated with the acute loss of these hormones. ROS-activated FoxOs in early mesenchymal progenitors also divert ss-catenin away from Wn...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149731</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
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            <title>Molecular Aspects of Thyroid Hormone Actions.</title>
            <link>http://www.medworm.com/index.php?rid=3149730&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051527%26dopt%3DAbstract</link>
            <description>Authors: Cheng SY, Leonard JL, Davis PJ
    Cellular actions of thyroid hormone may be initiated within the cell nucleus, at the plasma membrane, in cytoplasm, and at the mitochondrion. Thyroid hormone nuclear receptors (TRs) mediate the biological activities of T3 via transcriptional regulation. Two TR genes, alpha and beta, encode four T3-binding receptor isoforms (alpha1, beta1, beta2, and beta3). The transcriptional activity of TRs is regulated at multiple levels. Besides being regulated by T3, transcriptional activity is regulated by the type of thyroid hormone response elements located on the promoters of T3 target genes, by the developmental- and tissue-dependent expression of TR isoforms, and by a host of nuclear coregulatory proteins. These nuclear coregulatory proteins modulate t...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149730</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149730</guid>        </item>
        <item>
            <title>Estrogen Therapy and Cognition: A Review of the Cholinergic Hypothesis.</title>
            <link>http://www.medworm.com/index.php?rid=3106553&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20019127%26dopt%3DAbstract</link>
            <description>Authors: Gibbs RB
    The pros and cons of estrogen therapy for use in postmenopausal women continue to be a major topic of debate in women's health. Much of this debate focuses on the potential benefits vs. harm of estrogen therapy on the brain and the risks for cognitive impairment associated with aging and Alzheimer's disease. Many animal and human studies suggest that estrogens can have significant beneficial effects on brain aging and cognition and reduce the risk of Alzheimer's-related dementia; however, others disagree. Important discoveries have been made, and hypotheses have emerged that may explain some of the inconsistencies. This review focuses on the cholinergic hypothesis, specifically on evidence that beneficial effects of estrogens on brain aging and cognition are related t...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3106553</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3106553</guid>        </item>
        <item>
            <title>Can the Genetics of Type 1 and Type 2 Diabetes Shed Light on the Genetics of Latent Autoimmune Diabetes in Adults?</title>
            <link>http://www.medworm.com/index.php?rid=3101306&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20007922%26dopt%3DAbstract</link>
            <description>Authors: Grant SF, Hakonarson H, Schwartz S
    The pathophysiology of latent autoimmune diabetes in adults (LADA) is considered less understood than its much better characterized counterparts of type 1 and type 2 diabetes (T1D and T2D), where its clinical presentation exhibits some features of each of these two main diseases, earning it a reputation as being &quot;type 1.5 diabetes&quot;. The etiology of LADA remains unknown, but a genetic component has been implicated from recent reports of T1D and T2D genes playing a role in its pathogenesis. One way to shed much needed light on the classification of LADA is to determine the discrete genetic factors conferring risk to the pathogenesis of this specific phenotype and to determine to what extent LADA shares genetic similarities with T1D and T2D. For...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101306</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101306</guid>        </item>
        <item>
            <title>The Secret Life of NAD+: An Old Metabolite Controlling New Metabolic Signaling Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=3101307&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20007326%26dopt%3DAbstract</link>
            <description>Authors: Houtkooper RH, Cant&amp;#xF3; C, Wanders RJ, Auwerx J
    A century after the identification of a coenzymatic activity for NAD(+), NAD(+) metabolism has come into the spotlight again due to the potential therapeutic relevance of a set of enzymes whose activity is tightly regulated by the balance between the oxidized and reduced forms of this metabolite. In fact, the actions of NAD(+) have been extended from being an oxidoreductase cofactor for single enzymatic activities to acting as substrate for a wide range of proteins. These include NAD(+)-dependent protein deacetylases, poly(ADP-ribose) polymerases, and transcription factors that affect a large array of cellular functions. Through these effects, NAD(+) provides a direct link between the cellular redox status and the control of si...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101307</comments>
            <pubDate>Wed, 09 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101307</guid>        </item>
        <item>
            <title>Glucose Variability; Does It Matter?</title>
            <link>http://www.medworm.com/index.php?rid=3068081&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19966012%26dopt%3DAbstract</link>
            <description>Authors: Siegelaar SE, Holleman F, Hoekstra JB, Devries JH
    Overall lowering of glucose is of pivotal importance in the treatment of diabetes, with proven beneficial effects on microvascular and macrovascular outcomes. Still, patients with similar glycosylated hemoglobin levels and mean glucose values can have markedly different daily glucose excursions. The role of this glucose variability in pathophysiological pathways is the subject of debate. It is strongly related to oxidative stress in in vitro, animal, and human studies in an experimental setting. However, in real-life human studies including type 1 and type 2 diabetes patients, there is neither a reproducible relation with oxidative stress nor a correlation between short-term glucose variability and retinopathy, nephropathy, or ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3068081</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Sex Steroid Hormones, Hormonal Contraception, and the Immunobiology of Human Immunodeficiency Virus-1 Infection.</title>
            <link>http://www.medworm.com/index.php?rid=2986671&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19903932%26dopt%3DAbstract</link>
            <description>Authors: Hel Z, Stringer E, Mestecky J
    Worldwide, an increasing number of women use oral or injectable hormonal contraceptives. However, inadequate information is available to aid women and health care professionals in weighing the potential risks of hormonal contraceptive use in individuals living with HIV-1 or at high risk of infection. Numerous epidemiological studies and challenge studies in a rhesus macaque model suggest that progesterone-based contraceptives increase the risk of HIV-1 infection in humans and simian immunodeficiency virus (SIV) infection in macaques, accelerate disease progression, and increase viral shedding in the genital tract. However, because several other studies in humans have not observed any effect of exogenously administered progesterone on HIV-1 acquisi...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2986671</comments>
            <pubDate>Tue, 10 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2986671</guid>        </item>
        <item>
            <title>The Effects of Opioids and Opioid Analogs on Animal and Human Endocrine Systems.</title>
            <link>http://www.medworm.com/index.php?rid=2986670&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19903933%26dopt%3DAbstract</link>
            <description>Authors: Vuong C, Van Uum SH, O'Dell LE, Lutfy K, Friedman TC
    Opioid abuse has increased in the last decade, primarily as a result of increased access to prescription opioids. Physicians are also increasingly administering opioid analgesics for noncancer chronic pain. Thus, knowledge of the long-term consequences of opioid use/abuse has important implications for fully evaluating the clinical usefulness of opioid medications. Many studies have examined the effect of opioids on the endocrine system; however, a systematic review of the endocrine actions of opioids in both humans and animals has, to our knowledge, not been published since 1984. Thus, we reviewed the literature on the effect of opioids on the endocrine system. We included both acute and chronic effects of opioids, with the...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2986670</comments>
            <pubDate>Tue, 10 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2986670</guid>        </item>
        <item>
            <title>Small G Proteins in Islet {beta}-Cell Function.</title>
            <link>http://www.medworm.com/index.php?rid=2970756&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19890090%26dopt%3DAbstract</link>
            <description>Authors: Kowluru A
    Glucose-stimulated insulin secretion from the islet beta-cell involves a sequence of metabolic events and an interplay between a wide range of signaling pathways leading to the generation of second messengers (e.g., cyclic nucleotides, adenine and guanine nucleotides, soluble lipid messengers) and mobilization of calcium ions. Consequent to the generation of necessary signals, the insulin-laden secretory granules are transported from distal sites to the plasma membrane for fusion and release of their cargo into the circulation. The secretory granule transport underlies precise changes in cytoskeletal architecture involving a well-coordinated cross-talk between various signaling proteins, including small molecular mass GTP-binding proteins (G proteins) and their respe...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970756</comments>
            <pubDate>Wed, 04 Nov 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Crosstalk in Inflammation: The Interplay of Glucocorticoid Receptor-Based Mechanisms and Kinases and Phosphatases.</title>
            <link>http://www.medworm.com/index.php?rid=2970755&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19890091%26dopt%3DAbstract</link>
            <description>Authors: Beck IM, Vanden Berghe W, Vermeulen L, Yamamoto KR, Haegeman G, De Bosscher K
    Glucocorticoids (GCs) are steroidal ligands for the GC receptor (GR), which can function as a ligand-activated transcription factor. These steroidal ligands and derivatives thereof are the first line of treatment in a vast array of inflammatory diseases. However, due to the general surge of side effects associated with long-term use of GCs and the potential problem of GC resistance in some patients, the scientific world continues to search for a better understanding of the GC-mediated antiinflammatory mechanisms. The reversible phosphomodification of various mediators in the inflammatory process plays a key role in modulating and fine-tuning the sensitivity, longevity, and intensity of the inflammato...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970755</comments>
            <pubDate>Wed, 04 Nov 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Steroidogenesis in the Fetal Testis and Its Susceptibility to Disruption by Exogenous Compounds.</title>
            <link>http://www.medworm.com/index.php?rid=2970757&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887492%26dopt%3DAbstract</link>
            <description>Authors: Scott HM, Mason JI, Sharpe RM
    Masculinization depends on adequate production of testosterone by the fetal testis within a specific &quot;masculinization programming window.&quot; Disorders resulting from subtle deficiencies in this process are common in humans, and environmental exposures/lifestyle could contribute causally because common therapeutic and environmental compounds can affect steroidogenesis. This evidence derives mainly from rodent studies, but because there are major species differences in regulation of steroidogenesis in the fetal testis, this may not always be a guide to potential effects in the human. In addition to direct study of the effects of compounds on steroidogenesis, information also derives from study of masculinization disorders that result from mutations in...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970757</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>The Role of Mitochondria in the Pathophysiology of Skeletal Muscle Insulin Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=2939718&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861693%26dopt%3DAbstract</link>
            <description>Authors: Pagel-Langenickel I, Bao J, Pang L, Sack MN
    Multiple organs contribute to the development of peripheral insulin resistance, with the major contributors being skeletal muscle, liver, and adipose tissue. Because insulin resistance usually precedes the development of type 2 diabetes mellitus (T2DM) by many years, understanding the pathophysiology of insulin resistance should enable development of therapeutic strategies to prevent disease progression. Some subjects with mitochondrial genomic variants/defects and a subset of lean individuals with hereditary predisposition to T2DM exhibit skeletal muscle mitochondrial dysfunction early in the course of insulin resistance. In contrast, in the majority of subjects with T2DM the plurality of evidence implicates skeletal muscle mitochon...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939718</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
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            <title>Metabolism and Circadian Rhythms--Implications for Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=2931562&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19854863%26dopt%3DAbstract</link>
            <description>Authors: Froy O
    Obesity has become a serious public health problem and a major risk factor for the development of illnesses, such as insulin resistance and hypertension. Human homeostatic systems have adapted to daily changes in light and dark in a way that the body anticipates the sleep and activity periods. Mammals have developed an endogenous circadian clock located in the suprachiasmatic nuclei of the anterior hypothalamus that responds to the environmental light-dark cycle. Similar clocks have been found in peripheral tissues, such as the liver, intestine, and adipose tissue, regulating cellular and physiological functions. The circadian clock has been reported to regulate metabolism and energy homeostasis in the liver and other peripheral tissues. This is achieved by mediating th...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2931562</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
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            <title>Genetic Regulation of Pituitary Gland Development in Human and Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2905936&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19837867%26dopt%3DAbstract</link>
            <description>Authors: Kelberman D, Rizzoti K, Lovell-Badge R, Robinson IC, Dattani MT
    Normal hypothalamopituitary development is closely related to that of the forebrain and is dependent upon a complex genetic cascade of transcription factors and signaling molecules that may be either intrinsic or extrinsic to the developing Rathke's pouch. These factors dictate organ commitment, cell differentiation, and cell proliferation within the anterior pituitary. Abnormalities in these processes are associated with congenital hypopituitarism, a spectrum of disorders that includes syndromic disorders such as septo-optic dysplasia, combined pituitary hormone deficiencies, and isolated hormone deficiencies, of which the commonest is GH deficiency. The highly variable clinical phenotypes can now in part be expl...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905936</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2905936</guid>        </item>
        <item>
            <title>Effects of Intrauterine Exposure to Synthetic Glucocorticoids on Fetal, Newborn, and Infant Hypothalamic-Pituitary-Adrenal Axis Function in Humans: A Systematic Review.</title>
            <link>http://www.medworm.com/index.php?rid=2905935&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19837868%26dopt%3DAbstract</link>
            <description>Conclusions: This systematic review has allowed the demonstration of the way in which intrauterine exposure to various regimens of synthetic glucocorticoids affects various forms of hpa function. As such, it guides future studies in terms of which variables need to be focused on in order to further strengthen the understanding of such therapy, whilst continuing to profit from its clinical benefits.
    PMID: 19837868 [PubMed - as supplied by publisher] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905935</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2905935</guid>        </item>
        <item>
            <title>The Mammalian Ovary from Genesis to Revelation.</title>
            <link>http://www.medworm.com/index.php?rid=2832816&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19776209%26dopt%3DAbstract</link>
            <description>Authors: Edson MA, Nagaraja AK, Matzuk MM
    Two major functions of the mammalian ovary are the production of germ cells (oocytes), which allow continuation of the species, and the generation of bioactive molecules, primarily steroids (mainly estrogens and progestins) and peptide growth factors, which are critical for ovarian function, regulation of the hypothalamic-pituitary-ovarian axis, and development of secondary sex characteristics. The female germline is created during embryogenesis when the precursors of primordial germ cells differentiate from somatic lineages of the embryo and take a unique route to reach the urogenital ridge. This undifferentiated gonad will differentiate along a female pathway, and the newly formed oocytes will proliferate and subsequently enter meiosis. At th...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832816</comments>
            <pubDate>Tue, 22 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832816</guid>        </item>
        <item>
            <title>Kisspeptin Signaling in the Brain.</title>
            <link>http://www.medworm.com/index.php?rid=2825288&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19770291%26dopt%3DAbstract</link>
            <description>Authors: Oakley AE, Clifton DK, Steiner RA
    Kisspeptin (a product of the Kiss1 gene) and its receptor (GPR54 or Kiss1r) have emerged as key players in the regulation of reproduction. Mutations in humans or genetically targeted deletions in mice of either Kiss1 or Kiss1r cause profound hypogonadotropic hypogonadism. Neurons that express Kiss1/kisspeptin are found in discrete nuclei in the hypothalamus, as well as other brain regions in many vertebrates, and their distribution, regulation, and function varies widely across species. Kisspeptin neurons directly innervate and stimulate GnRH neurons, which are the final common pathway through which the brain regulates reproduction. Kisspeptin neurons are sexually differentiated with respect to cell number and transcriptional activity in certa...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2825288</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2825288</guid>        </item>
        <item>
            <title>Insulin Receptor Isoforms and Insulin Receptor/Insulin-Like Growth Factor Receptor Hybrids in Physiology and Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2801150&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19752219%26dopt%3DAbstract</link>
            <description>Authors: Belfiore A, Frasca F, Pandini G, Sciacca L, Vigneri R
    In mammals, the insulin receptor (IR) gene has acquired an additional exon, exon 11. This exon may be skipped in a developmental and tissue-specific manner. The IR, therefore, occurs in two isoforms (exon 11 minus IR-A and exon 11 plus IR-B). The most relevant functional difference between these two isoforms is the high affinity of IR-A for IGF-II. IR-A is predominantly expressed during prenatal life. It enhances the effects of IGF-II during embryogenesis and fetal development. It is also significantly expressed in adult tissues, especially in the brain. Conversely, IR-B is predominantly expressed in adult, well-differentiated tissues, including the liver, where it enhances the metabolic effects of insulin. Dysregulation of...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2801150</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2801150</guid>        </item>
        <item>
            <title>Pathomechanisms of Type 2 Diabetes Genes.</title>
            <link>http://www.medworm.com/index.php?rid=2801151&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19749172%26dopt%3DAbstract</link>
            <description>Authors: Staiger H, Machicao F, Fritsche A, H&amp;#xE4;ring HU
    Type 2 diabetes mellitus is a complex metabolic disease that is caused by insulin resistance and beta-cell dysfunction. Furthermore, type 2 diabetes has an evident genetic component and represents a polygenic disease. During the last decade, considerable progress was made in the identification of type 2 diabetes risk genes. This was crucially influenced by the development of affordable high-density single nucleotide polymorphism (SNP) arrays that prompted several successful genome-wide association scans in large case-control cohorts. Subsequent to the identification of type 2 diabetes risk SNPs, cohorts thoroughly phenotyped for prediabetic traits with elaborate in vivo methods allowed an initial characterization of the pathome...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2801151</comments>
            <pubDate>Thu, 10 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2801151</guid>        </item>
        <item>
            <title>The Endocrine Society Laureate Awards.</title>
            <link>http://www.medworm.com/index.php?rid=2692776&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19663075%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19663075 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692776</comments>
            <pubDate>Fri, 31 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2692776</guid>        </item>
        <item>
            <title>The Endocrine Society 2009 Laureate Awards.</title>
            <link>http://www.medworm.com/index.php?rid=2692775&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19663077%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19663077 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692775</comments>
            <pubDate>Fri, 31 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2692775</guid>        </item>
        <item>
            <title>The Role of Liver-Derived IGF-I.</title>
            <link>http://www.medworm.com/index.php?rid=2593365&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19589948%26dopt%3DAbstract</link>
            <description>Authors: Ohlsson C, Mohan S, Sj&amp;#xF6;gren K, Tivesten A, Isgaard J, Isaksson O, Jansson JO, Svensson J
    Insulin-like growth factor-I (IGF-I) is expressed in virtually every tissue of the body but with much higher expression in the liver than in any other tissue. Studies using mice with liver-specific IGF-I knock out (KO) have demonstrated that liver-derived IGF-I, constituting a major part of circulating IGF-I, is an important endocrine factor involved in a variety of physiological and pathological processes. Detailed studies comparing the impact of liver-derived IGF-I and local bone-derived IGF-I demonstrate that both sources of IGF-I can stimulate longitudinal bone growth. We propose here that liver-derived circulating IGF-I and local bone-derived IGF-I to some extent have overlapping...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2593365</comments>
            <pubDate>Wed, 08 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2593365</guid>        </item>
        <item>
            <title>Ovarian Ageing: Mechanisms and Clinical Consequences.</title>
            <link>http://www.medworm.com/index.php?rid=2593364&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19589949%26dopt%3DAbstract</link>
            <description>Authors: Broekmans FJ, Soules MR, Fauser BC
    The cessation of menstrual cycles at a mean age of 50 and increasing longevity imply that women spend almost half of their lives in a postmenopausal status. Menopause can be seen as a fulcrum for several health risks, like infertility and several estrogen dependent disease states. It is the final step in the process referred to as ovarian ageing. The mechanisms behind this ageing process are not well understood. The present review puts effort in describing the various phases of ovarian ageing and the markers that express the ovarian changes over time when clinical signs are still absent. The endocrine changes that occur in paralellel to changes in cycle regularity are summarised, as they underline the key changes in ovarian function. The timi...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2593364</comments>
            <pubDate>Wed, 08 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2593364</guid>        </item>
        <item>
            <title>Molecular Mechanisms Underlying the Activation of Mammalian Primordial Follicles.</title>
            <link>http://www.medworm.com/index.php?rid=2593363&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19589950%26dopt%3DAbstract</link>
            <description>Authors: Adhikari D, Liu K
    In humans and other mammalian species, the pool of resting primordial follicles serves as the source of developing follicles and fertilizable ova for the entire length of female reproductive life. One question that has intrigued biologists is the mechanisms controlling the activation of dormant primordial follicles. Studies from previous decades have laid a solid, but yet incomplete, foundation. In recent years, molecular mechanisms underlying follicular activation have become more evident, mainly through the use of genetically-modified mouse models. As hypothesized in the 1990s, the pool of primordial follicles is now known to be maintained in a dormant state by various forms of inhibitory machinery, which are provided by several inhibitory signals and molec...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2593363</comments>
            <pubDate>Wed, 08 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2593363</guid>        </item>
        <item>
            <title>History of aromatase: saga of an important biological mediator and therapeutic target.</title>
            <link>http://www.medworm.com/index.php?rid=2533151&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19389994%26dopt%3DAbstract</link>
            <description>Authors: Santen RJ, Brodie H, Simpson ER, Siiteri PK, Brodie A
    Aromatase is the enzyme that catalyzes the conversion of androgens to estrogens. Initial studies of its enzymatic activity and function took place in an environment focused on estrogen as a component of the birth control pill. At an early stage, investigators recognized that inhibition of this enzyme could have major practical applications for treatment of hormone-dependent breast cancer, alterations of ovarian and endometrial function, and treatment of benign disorders such as gynecomastia. Two general approaches ultimately led to the development of potent and selective aromatase inhibitors. One targeted the enzyme using analogs of natural steroidal substrates to work out the relationships between structure and function. T...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533151</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533151</guid>        </item>
        <item>
            <title>Iodine deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=2533144&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19460960%26dopt%3DAbstract</link>
            <description>Authors: Zimmermann MB
    Iodine deficiency has multiple adverse effects in humans, termed iodine deficiency disorders, due to inadequate thyroid hormone production. Globally, it is estimated that 2 billion individuals have an insufficient iodine intake, and South Asia and sub-Saharan Africa are particularly affected. However, about 50% of Europe remains mildly iodine deficient, and iodine intakes in other industrialized countries, including the United States and Australia, have fallen in recent years. Iodine deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary iodine concentration, goiter, newborn...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533144</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533144</guid>        </item>
        <item>
            <title>Endocrine-disrupting chemicals: an Endocrine Society scientific statement.</title>
            <link>http://www.medworm.com/index.php?rid=2533140&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19502515%26dopt%3DAbstract</link>
            <description>Authors: Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, Zoeller RT, Gore AC
    There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533140</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533140</guid>        </item>
        <item>
            <title>Unraveling IGFBP-3 Actions in Human Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2533142&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477944%26dopt%3DAbstract</link>
            <description>Authors: Jogie-Brahim S, Feldman D, Oh Y
    The IGF system plays critical roles in somatic growth in an endocrine fashion (somatomedin hypothesis) as well as proliferation and differentiation of normal and malignant cells in a paracrine/autocrine fashion. IGFBP-3 is known to modulate the actions of IGFs in circulation as well as the immediate extracellular environment. Interestingly, apart from the ability to inhibit or enhance IGF actions, IGFBP-3 also exhibits very clear, distinct biologic effects independent of the IGF/IGF-I receptor axis. Over the past decade it has become widely appreciated that IGF/IGF-IR-independent actions of IGFBP-3 (antiproliferative and pro-apoptotic effects) contribute to improving the pathophysiology of a variety of human diseases such as cancer, diabetes and...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533142</comments>
            <pubDate>Wed, 27 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533142</guid>        </item>
        <item>
            <title>Instructing an embryonic stem cell-derived oocyte fate: lessons from endogenous oogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2533155&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19366753%26dopt%3DAbstract</link>
            <description>Authors: Nicholas CR, Chavez SL, Baker VL, Reijo Pera RA
    Female reproductive potential is limited in the majority of species due to oocyte depletion. Because functional human oocytes are restricted in number and accessibility, a robust system to differentiate oocytes from stem cells would enable a thorough investigation of the genetic, epigenetic, and environmental factors affecting human oocyte development. Also, the differentiation of functional oocytes from stem cells may permit the success of human somatic cell nuclear transfer for reprogramming studies and for the production of patient-specific embryonic stem cells (ESCs). Thus, ESC-derived oocytes could ultimately help to restore fertility in women. Here, we review endogenous and ESC-derived oocyte development, and we discuss the...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533155</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533155</guid>        </item>
        <item>
            <title>Ethical issues in stem cell research.</title>
            <link>http://www.medworm.com/index.php?rid=2533153&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19366754%26dopt%3DAbstract</link>
            <description>This article provides a critical analysis of these issues and how they are addressed in current policies.
    PMID: 19366754 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533153</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533153</guid>        </item>
        <item>
            <title>Stem cells to pancreatic beta-cells: new sources for diabetes cell therapy.</title>
            <link>http://www.medworm.com/index.php?rid=2533149&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19389995%26dopt%3DAbstract</link>
            <description>Authors: Guo T, Hebrok M
    The number of patients worldwide suffering from the chronic disease diabetes mellitus is growing at an alarming rate. Insulin-secreting beta-cells in the islet of Langerhans are damaged to different extents in diabetic patients, either through an autoimmune reaction present in type 1 diabetic patients or through inherent changes within beta-cells that affect their function in patients suffering from type 2 diabetes. Cell replacement strategies via islet transplantation offer potential therapeutic options for diabetic patients. However, the discrepancy between the limited number of donor islets and the high number of patients who could benefit from such a treatment reflects the dire need for renewable sources of high-quality beta-cells. Human embryonic stem cell...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533149</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533149</guid>        </item>
        <item>
            <title>In search of adrenocortical stem and progenitor cells.</title>
            <link>http://www.medworm.com/index.php?rid=2533148&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19403887%26dopt%3DAbstract</link>
            <description>We present evidence for the existence and location of adrenocortical stem/progenitor cells and their potential contribution to adrenocortical carcinomas. Data described herein come primarily from studies conducted in the Hammer laboratory with incorporation of important related studies from other investigators. Together, the work provides a framework for the emerging somatic stem cell field as it relates to the adrenal gland.
    PMID: 19403887 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533148</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533148</guid>        </item>
        <item>
            <title>Editorial: Update on stem cell research.</title>
            <link>http://www.medworm.com/index.php?rid=2533146&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433633%26dopt%3DAbstract</link>
            <description>Authors: Robertson RP, Giudice LC
    
    PMID: 19433633 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533146</comments>
            <pubDate>Thu, 30 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533146</guid>        </item>
        <item>
            <title>Thyrotropin and homologous glycoprotein hormone receptors: structural and functional aspects of extracellular signaling mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=2533162&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176466%26dopt%3DAbstract</link>
            <description>Authors: Kleinau G, Krause G
    The TSH receptor (TSHR) together with the homologous lutropin/choriogonadotropin receptor and the follitropin receptor are glycoprotein hormone receptors (GPHRs). They constitute a subfamily of the rhodopsin-like G protein-coupled receptors with seven transmembrane helices. GPHRs and their corresponding hormones are pivotal proteins with respect to a variety of physiological functions. The identification and characterization of intra- and intermolecular signaling determinants as well as signaling mechanisms are prerequisites to gaining molecular insights into functions and (pathogenic) dysfunctions of GPHRs. Knowledge about activation mechanisms is fragmentary, and the specific aspects have still not been understood in their entirety. Therefore, here we cri...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533162</comments>
            <pubDate>Tue, 31 Mar 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533162</guid>        </item>
        <item>
            <title>The role of the calcium-sensing receptor in the development and progression of cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2533159&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19237714%26dopt%3DAbstract</link>
            <description>Authors: Saidak Z, Mentaverri R, Brown EM
    The calcium-sensing receptor (CaR) is responsive to changes in the extracellular Ca(2+) (Ca(2+)(o)) concentration. It is a member of the largest family of cell surface receptors, the G protein-coupled receptors, and it has been shown to be involved in Ca(2+)(o) homeostasis. Apart from its primary role in Ca(2+)(o) homeostasis, the CaR may be involved in phenomena that allow for the development of many types of benign or malignant tumors, from parathyroid adenomas to breast, prostate, and colon cancers. For example, whereas the CaR is expressed in both normal and malignant breast tissue, increased CaR levels have been reported in highly metastatic primary breast cancer cells and breast cancer cell lines, possibly contributing to their malignancy...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533159</comments>
            <pubDate>Tue, 31 Mar 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533159</guid>        </item>
        <item>
            <title>Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects.</title>
            <link>http://www.medworm.com/index.php?rid=2533157&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19240267%26dopt%3DAbstract</link>
            <description>Authors: M&amp;#xF8;ller N, J&amp;#xF8;rgensen JO
    In evolutionary terms, GH and intracellular STAT 5 signaling is a very old regulatory system. Whereas insulin dominates periprandially, GH may be viewed as the primary anabolic hormone during stress and fasting. GH exerts anabolic effects directly and through stimulation of IGF-I, insulin, and free fatty acids (FFA). When subjects are well nourished, the GH-induced stimulation of IGF-I and insulin is important for anabolic storage and growth of lean body mass (LBM), adipose tissue, and glycogen reserves. During fasting and other catabolic states, GH predominantly stimulates the release and oxidation of FFA, which leads to decreased glucose and protein oxidation and preservation of LBM and glycogen stores. The most prominent metabolic effect of ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533157</comments>
            <pubDate>Tue, 31 Mar 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2533157</guid>        </item>
        <item>
            <title>Trophoblast Stem Cells: Models for Investigating Trophectoderm Differentiation and Placental Development.</title>
            <link>http://www.medworm.com/index.php?rid=2288137&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19299251%26dopt%3DAbstract</link>
            <description>Authors: Douglas GC, Vandevoort C, Kumar P, Chang TC, Golos TG
    The placenta is an ephemeral organ, containing diverse populations of trophoblasts which are all derived from the embryonic trophectoderm, but which have morphological, functional and molecular diversity within and across species. In hemochorial placentation these cells play especially important roles interfacing with, and modifying the cells of the maternal decidua. Within the rapidly growing placenta, it has been shown that there are trophoblast stem cells (TSC), well characterized in the mouse, and postulated but not well-understood in primates. This review will discuss the characteristics of candidates for human and nonhuman primate TSC, present the diverse methods of their generation, and propose future prospects for e...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2288137</comments>
            <pubDate>Wed, 18 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2288137</guid>        </item>
        <item>
            <title>Effects of Growth Hormone on Glucose, Lipid and Protein Metabolism in Human Subjects.</title>
            <link>http://www.medworm.com/index.php?rid=2221174&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19240267%26dopt%3DAbstract</link>
            <description>Authors: M&amp;#xF8;ller N, Otto Lunde J&amp;#xF8;rgensen J
    In evolutionary terms growth hormone (GH) and intracellular STAT 5 signaling is a very old regulatory system. Whereas insulin dominates peri-prandially, GH may be viewed as the primary anabolic hormone during stress and fasting. GH exerts anabolic effects directly and through stimulation of IGF-I, insulin, and free fatty acids (FFA). When well nourished the GH-induced stimulation of IGF-I and insulin is important for anabolic storage and growth of lean body mass (LBM), adipose tissue and glycogen reserves. During fasting and other catabolic states GH predominantly stimulates the release and oxidation of FFA which leads to decreased glucose and protein oxidation and preservation of LBM and glycogen stores. The most prominent metabolic ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221174</comments>
            <pubDate>Tue, 24 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2221174</guid>        </item>
        <item>
            <title>The Role of the Calcium Sensing Receptor in the Development and Progression of Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2215368&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19237714%26dopt%3DAbstract</link>
            <description>Authors: Saidak Z, Mentaverri R, Brown EM
    The Calcium sensing Receptor (CaR) is responsive to changes in the extracellular Ca(2+) concentration (Ca(2+)o). It is a member of the largest family of cell surface receptors, the G protein-coupled receptors (GPCRs), and it has been shown to be involved in Ca(2+)o homeostasis. Apart from its primary role in Ca(2+)o homeostasis, the CaR may be involved in phenomena that allow for the development of many types of benign or malignant tumors, from parathyroid adenomas to breast, prostate and colon cancers. For example, while the CaR is expressed in both normal and malignant breast tissue, increased CaR levels have been reported in highly metastatic primary breast cancer cells and breast cancer cell lines, possibly contributing to their malignancy ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2215368</comments>
            <pubDate>Mon, 23 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2215368</guid>        </item>
        <item>
            <title>Thyrotropin- and Homologous Glycoprotein Hormone Receptors: Structural and Functional Aspects of Extracellular Signaling Mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=2146879&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176466%26dopt%3DAbstract</link>
            <description>Authors: Kleinau G, Krause G
    The thyrotropin receptor (TSHR) together with the homologous lutropin/choriogonadotropin (LHCGR) and the follitropin receptor (FSHR) are glycoprotein-hormone receptors (GPHRs). They constitute a subfamily of the rhodopsin-like G-protein coupled receptors (GPCRs) with seven transmembrane helices. GPHRs and their corresponding hormones are pivotal proteins with respect to a variety of physiological functions. The identification and characterization of intra- and intermolecular signaling determinants as well as signaling-mechanisms are prerequisites to gaining molecular insights into functions and (pathogenic) dysfunctions of GPHRs. Knowledge about activation mechanisms is fragmentary and the specific aspects have still not been understood in their entirety. T...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146879</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146879</guid>        </item>
        <item>
            <title>Androgen Receptor Roles in Spermatogenesis and Fertility: Lessons from Testicular Cell-Specific Androgen Receptor Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2146878&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176467%26dopt%3DAbstract</link>
            <description>Authors: Wang RS, Yeh S, Tzeng CR, Chang C
    Androgens are critical steroid hormones that determine the expression of the male phenotype, including the outward development of secondary sex characteristics as well as the initiation and maintenance of spermatogenesis. Their actions are mediated by the androgen receptor (AR), a member of the nuclear receptor superfamily. AR functions as a ligand-dependent transcription factor, regulating expression of an array of androgen-responsive genes. Androgen and the AR play important roles in male spermatogenesis and fertility. The recent generation and characterization of male total and conditional AR knockout (AR(-/y)) mice from different laboratories demonstrated the necessity of AR signaling for both external and internal male phenotype developme...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146878</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146878</guid>        </item>
        <item>
            <title>Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes?</title>
            <link>http://www.medworm.com/index.php?rid=2120337&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151107%26dopt%3DAbstract</link>
            <description>Authors: Johnson RJ, Perez-Pozo SE, Sautin YY, Manitius J, Sanchez-Lozada LG, Feig DI, Shafiu M, Segal M, Glassock RJ, Shimada M, Roncal C, Nakagawa T
    We propose that excessive fructose intake (&amp;gt;50 g/day) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup (HFCS). First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there is now extensive experimental and clinical data supporting uric acid in the pathogenesis of meta...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120337</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2120337</guid>        </item>
        <item>
            <title>Growth Hormone and Insulin-Like Growth Factor-I in the Transition from Normal Mammary Development to Preneoplastic Mammary Lesions.</title>
            <link>http://www.medworm.com/index.php?rid=2045342&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19075184%26dopt%3DAbstract</link>
            <description>Authors: Kleinberg DL, Wood TL, Furth PA, Lee AV
    Adult female mammary development starts at puberty and is controlled by tightly regulated cross-talk between a group of hormones and growth factors. Although estrogen is the initial driving force, and is joined by luteal phase progesterone, both of these hormones require growth hormone induced IGF-I in the mammary gland in order to act. The same group of hormones, when experimentally perturbed, can lead to development of hyperplastic lesions and increase the chances, or be precursors, of mammary carcinoma. For example, systemic administration of growth hormone (GH) or IGF-I causes mammary hyperplasia, and overproduction of IGF-I in transgenic animals can cause the development of usual or atypical hyperplasias and sometimes carcinoma. Whi...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2045342</comments>
            <pubDate>Mon, 15 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2045342</guid>        </item>
        <item>
            <title>Bisphenol-A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption.</title>
            <link>http://www.medworm.com/index.php?rid=2045343&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19074586%26dopt%3DAbstract</link>
            <description>Authors: Vandenberg LN, Maffini MV, Sonnenschein C, Rubin BS, Soto AM
    In 1991, a group of 21 scientists gathered at the Wingspread Conference center to discuss evidence of developmental alterations observed in wildlife populations following chemical exposures. There, the term &quot;endocrine disruptor&quot; was agreed upon to describe a class of chemicals including those that act as agonists and antagonists of the estrogen receptors, androgen receptor, thyroid hormone receptor, and others. This definition has since evolved and the field has grown to encompass hundreds of chemicals. In spite of significant advances in the study of endocrine disruptors, several controversies have sprung up and continue, including the debate over the existence of non-monotonic dose response curves, the mechanisms o...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2045343</comments>
            <pubDate>Fri, 12 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2045343</guid>        </item>
        <item>
            <title>Evidence-Based and Potential Benefits of Metformin in the Polycystic Ovary Syndrome: A Comprehensive Review.</title>
            <link>http://www.medworm.com/index.php?rid=2016030&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056992%26dopt%3DAbstract</link>
            <description>Authors: Palomba S, Falbo A, Zullo F, Orio Jr F
    Metformin is an insulin sensitizer widely used for the treatment of patients affected by type-2 diabetes mellitus. Since many women with polycystic ovary syndrome (PCOS) are insulin resistant, metformin was introduced in clinical practice to also treat these patients. Moreover, metformin's effect has other targets beside its insulin-sensitizing action. The present review was aimed to describe all evidence-based and potential employments of metformin in PCOS patients. In particular, will be analyzed not only the uses of metformin for the treatment of all PCOS-related disturbances such as menstrual disorders, anovulatory infertility, increased abortion or complicated pregnancy risk, hyperandrogenism, endometrial, metabolic and cardiovascula...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2016030</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2016030</guid>        </item>
        <item>
            <title>The Metabolic Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=1923637&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18971485%26dopt%3DAbstract</link>
            <description>Authors: Cornier MA, Dabelea D, Hernandez TL, Lindstrom RC, Steig AJ, Stob NR, Van Pelt RE, Wang H, Eckel RH
    The 'Metabolic Syndrome' (MetS) is a clustering of components that reflect overnutrition, sedentary lifestyles, and resultant excess adiposity. The MetS includes the clustering of abdominal obesity, insulin resistance, dyslipidemia, and elevated blood pressure and is associated with other comorbidities including the prothrombotic state, proinflammatory state, nonalcoholic fatty liver disease, and reproductive disorders. Because the MetS is a cluster of different conditions, and not a single disease, the development of multiple concurrent definitions has resulted. The prevalence of the MetS is increasing to epidemic proportions not only in the United States and the remainder of t...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1923637</comments>
            <pubDate>Wed, 29 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1923637</guid>        </item>
        <item>
            <title>Motivations and Methods for Analyzing Pulsatile Hormone Secretion.</title>
            <link>http://www.medworm.com/index.php?rid=1904998&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18940916%26dopt%3DAbstract</link>
            <description>Authors: Veldhuis JD, Keenan DM, Pincus SM
    Endocrine glands communicate with remote target cells via mixture of continuous and intermittent signal exchange. Continuous signaling allows slowly varying control, whereas intermittency permits rapid large adjustments. The control systems that mediate such homeostatic corrections operate in a species-, gender-, age- and context-selective fashion. Significant progress has been made in understanding mechanisms of adaptive interglandular signaling in vivo. Principal goals are to understand the physiological origins, significance and mechanisms of pulsatile hormone secretion. Key analytical issues are to (i) quantify the number, size, shape and uniformity of pulses, nonpulsatile (basal) secretion and elimination kinetics, (ii) evaluate regulatio...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1904998</comments>
            <pubDate>Tue, 21 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1904998</guid>        </item>
        <item>
            <title>The cap superfamily: cysteine-rich secretory proteins, antigen 5 and pathogenesis-related 1 proteins - roles in reproduction, cancer and immune defense.</title>
            <link>http://www.medworm.com/index.php?rid=1843745&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18824526%26dopt%3DAbstract</link>
            <description>THE CAP SUPERFAMILY: CYSTEINE-RICH SECRETORY PROTEINS, ANTIGEN 5 AND PATHOGENESIS-RELATED 1 PROTEINS - ROLES IN REPRODUCTION, CANCER AND IMMUNE DEFENSE.
    Endocr Rev. 2008 Sep 29;
    Authors: Gibbs GM, Roelants K, O'Bryan MK
    The cysteine-rich secretory proteins, antigen 5 and pathogenesis-related 1 proteins (CAP) superfamily members are found in a remarkable range of organisms spanning each of the animal kingdoms. Within humans and mice there are 31 and 33 individual family members respectively, and although many are poorly characterized, the majority show a notable expression bias to the reproductive tract, immune tissues or are deregulated in cancers. CAP superfamily proteins are most often secreted and have an extracellular endocrine or paracrine function and are involved in proc...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1843745</comments>
            <pubDate>Mon, 29 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1843745</guid>        </item>
        <item>
            <title>Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=1832415&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18815314%26dopt%3DAbstract</link>
            <description>Authors: Gereben B, Zavacki AM, Ribich S, Kim BW, Huang SA, Simonides WS, Ze&amp;#xF6;ld A, Bianco AC
    The iodothyronine deiodinases initiate or terminate thyroid hormone action, and therefore are critical for the biological effects mediated by thyroid hormone. Over the years research has focused on their role in preserving serum levels of the biologically active molecule triiodothyronine (T3) during iodine deficiency. More recently, a fascinating new role of these enzymes has been unveiled. The activating deiodinase (D2) and the inactivating deiodinase (D3) can locally increase or decrease thyroid hormone signaling in a tissue- and temporal-specific fashion, independently of changes in thyroid hormone serum concentrations. This mechanism is particularly relevant as deiodinase expression ca...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1832415</comments>
            <pubDate>Wed, 24 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1832415</guid>        </item>
        <item>
            <title>Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=1778475&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18776148%26dopt%3DAbstract</link>
            <description>JOINT GENETIC SUSCEPTIBILITY TO TYPE 1 DIABETES AND AUTOIMMUNE THYROIDITIS: FROM EPIDEMIOLOGY TO MECHANISMS.
    Endocr Rev. 2008 Sep 5;
    Authors: Huber A, Menconi F, Corathers S, Jacobson EM, Tomer Y
    Type 1 diabetes (T1D) and autoimmune thyroid diseases (AITD) frequently occur together within families and in the same individual. The co-occurrence of T1D+AITD in the same patient is one of the variants of the autoimmune polyglandular syndrome type 3 (APS3 variant [APS3v]). Epidemiological data point to a strong genetic influence on the shared susceptibility to T1D and AITD. Recently, significant progress has been made in our understanding of the genetic association between T1D and AITD. At least 3 genes have been confirmed as major joint susceptibility genes for T1D and AITD, HLA cla...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1778475</comments>
            <pubDate>Fri, 05 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1778475</guid>        </item>
        <item>
            <title>Causes and Metabolic Consequences of Fatty Liver.</title>
            <link>http://www.medworm.com/index.php?rid=1745164&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18723451%26dopt%3DAbstract</link>
            <description>Authors: Stefan N, Kantartzis K, H&amp;#xE4;ring HU
    Type 2 diabetes and cardiovascular disease represent a serious threat to the health of the population worldwide. While overall adiposity and particularly visceral adiposity are established risk factors for these diseases, in the recent years fatty liver emerged as an additional and independent factor. However, the pathophysiology of fat accumulation in the liver and the cross-talk of fatty liver with other tissues involved in metabolism in humans are not fully understood. Here we discuss the mechanisms involved in the pathogenesis of hepatic fat accumulation, particularly the roles of body fat distribution, nutrition, exercise, genetics and gene-environment interaction. Furthermore, the effects of fatty liver on glucose and lipid metaboli...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1745164</comments>
            <pubDate>Thu, 21 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1745164</guid>        </item>
        <item>
            <title>Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice.</title>
            <link>http://www.medworm.com/index.php?rid=1704242&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18694980%26dopt%3DAbstract</link>
            <description>Authors: Bouillon R, Carmeliet G, Verlinden L, van Etten E, Verstuyf A, Luderer HF, Lieben L, Mathieu C, Demay M
    The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1alpha-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1704242</comments>
            <pubDate>Mon, 11 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1704242</guid>        </item>
        <item>
            <title>Resolving the Conundrum of Islet Transplantation by Linking Metabolic Dysregulation, Inflammation, and Immune Regulation.</title>
            <link>http://www.medworm.com/index.php?rid=1670860&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18664617%26dopt%3DAbstract</link>
            <description>Authors: Huang X, Moore DJ, Ketchum RJ, Nunemaker CS, Kovatchev B, McCall AL, Brayman KL
    While Type 1 diabetes (T1D) cannot be prevented or reversed, replacement of insulin production by transplantation of the pancreas or pancreatic islets represents a definitive solution. At present, transplantation can restore euglycemia, but this restoration is short-lived, requires islets from multiple donors, and necessitates life-long immunosuppression. An emerging paradigm in transplantation and autoimmunity indicates that systemic inflammation contributes to tissue injury while disrupting immune tolerance. We identify multiple barriers to successful islet transplantation each of which either contributes to the inflammatory state or is augmented by it. To optimize islet transplantation for diabe...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1670860</comments>
            <pubDate>Tue, 29 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1670860</guid>        </item>
        <item>
            <title>Transcriptional Control of Energy Homeostasis by the Estrogen-Related Receptors (ERRs).</title>
            <link>http://www.medworm.com/index.php?rid=1670859&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18664618%26dopt%3DAbstract</link>
            <description>Authors: Gigu&amp;#xE8;re V
    Transcriptional control of cellular energy metabolic pathways is achieved by the coordinated action of numerous transcription factors and associated coregulators. Several members of the nuclear receptor superfamily have been shown to play important roles in this process as they can translate hormonal, nutrient and metabolite signals into specific gene expression networks to satisfy energy demands in response to distinct physiological cues. Estrogen-related receptor (ERR) alpha, ERRbeta and ERRgamma are nuclear receptors that have yet to be associated with a natural ligand, and are thus considered as orphan receptors. However, the transcriptional activity of the ERRs is exquisitely sensitive to the presence of coregulatory proteins known to be essential for the c...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1670859</comments>
            <pubDate>Tue, 29 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1670859</guid>        </item>
        <item>
            <title>{alpha}-Melanocyte-stimulating hormone and related tripeptides Biochemistry, anti-inflammatory and protective effects in vitro and in vivo and future perspectives for the treatment of immune-mediated inflammatory diseases.</title>
            <link>http://www.medworm.com/index.php?rid=1605097&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18612139%26dopt%3DAbstract</link>
            <description>Authors: Brzoska T, Luger TA, Maaser C, Abels C, B&amp;#xF6;hm M
    alpha-Melanocyte-stimulating hormone (alpha-MSH) is a tridecapeptide derived from the proopiomelanocortin. Many studies over the last years have provided evidence that alpha-MSH has potent protective and anti-inflammatory effects. These effects can be elicited via centrally expressed melanocortin receptors which orchestrate descending neurogenic anti- inflammatory pathways. alpha-MSH can also exert anti-inflammatory and protective effects on cells of the immune system and on peripheral non-immune cell types expressing melanocortin receptors. At the molecular level, alpha-MSH affects various pathways implicated in regulation of inflammation and protection, i. e. NF-kappaB activation, expression of adhesion molecules and chemok...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1605097</comments>
            <pubDate>Tue, 08 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1605097</guid>        </item>
        <item>
            <title>Glycerolipid metabolism and signaling in health and disease.</title>
            <link>http://www.medworm.com/index.php?rid=1602261&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18606873%26dopt%3DAbstract</link>
            <description>GLYCEROLIPID METABOLISM AND SIGNALING IN HEALTH AND DISEASE.
    Endocr Rev. 2008 Jul 8;
    Authors: Prentki M, Murthy Madiraju SR
    Maintenance of body temperature is achieved partly by modulating lipolysis by a network of complex regulatory mechanisms. Lipolysis is an integral part of the glycerolipid/free fatty acid (GL/FFA) cycle, which is the focus of this review and we discuss the significance of this pathway in the regulation of many physiological processes besides thermogenesis. GL/FFA cycle is referred to as a &quot;futile&quot; cycle as it involves continuous formation and hydrolysis of GL with the release of heat, at the expense of ATP. However, we present evidence underscoring the &quot;vital&quot; cellular signaling roles of the GL/FFA cycle for many biological processes. Probably because of i...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1602261</comments>
            <pubDate>Tue, 08 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1602261</guid>        </item>
        <item>
            <title>Clinical, Agricultural and Evolutionary Biology of Myostatin; a Comparative Review.</title>
            <link>http://www.medworm.com/index.php?rid=1563166&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18591260%26dopt%3DAbstract</link>
            <description>Authors: Rodgers BD, Garikipati DK
    The discovery of myostatin and our introduction to the &quot;Mighty Mouse&quot; over a decade ago has spurred both basic and applied research and has impacted popular culture as well. The myostatin null genotype produces &quot;double muscling&quot; in mice and livestock and was recently described in a child. The field's rapid growth is by no means surprising considering the potential benefits of enhancing muscle growth in clinical and agricultural settings. Indeed, several recent studies suggest that blocking myostatin's inhibitory effects could improve the clinical treatment of several muscle growth disorders while comparative studies suggest that these actions are at least partly conserved. Thus, neutralizing myostatin's effects could also have agricultural significanc...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1563166</comments>
            <pubDate>Mon, 30 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1563166</guid>        </item>
        <item>
            <title>Osteoporosis in Men.</title>
            <link>http://www.medworm.com/index.php?rid=1418223&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18451258%26dopt%3DAbstract</link>
            <description>Authors: Khosla S, Amin S, Orwoll E
    With the aging of the population, there is a growing recognition that osteoporosis and fractures in men are a significant public health problem, and both hip and vertebral fractures are associated with increased morbidity and mortality in men. Osteoporosis in men is a heterogeneous clinical entity: while most men experience bone loss with aging, some men develop osteoporosis at a relatively young age, often for unexplained reasons (idiopathic osteoporosis). Declining sex steroid levels and other hormonal changes likely contribute to age-related bone loss, as do impairments in osteoblast number and/or activity. Secondary causes of osteoporosis also play a significant role in pathogenesis. While there is ongoing controversy regarding whether osteoporos...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1418223</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1418223</guid>        </item>
        <item>
            <title>Osteoimmunology: Interactions of the Bone and Immune System.</title>
            <link>http://www.medworm.com/index.php?rid=1418222&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18451259%26dopt%3DAbstract</link>
            <description>Authors: Lorenzo J, Horowitz M, Choi Y
    Bone and the immune system are both complex tissues that respectively regulate the skeleton and the body's response to invading pathogens. It has now become clear that these organ systems often interact in their function. This is particularly true for the development of immune cells in the bone marrow and for the function of bone cells in health and disease. Because these two disciplines developed independently, investigators in each don't always fully appreciate the significance of the other system on the function of the tissue that they are studying. This review is meant to provide a broad overview of the many ways that bone and immune cells interact so that a better understanding of the role that each plays in the development and function of th...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1418222</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1418222</guid>        </item>
        <item>
            <title>Sphingolipids, Insulin Resistance, and Metabolic Disease: New Insights from in Vivo Manipulaton of Sphingolipid Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=1418221&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18451260%26dopt%3DAbstract</link>
            <description>Authors: Holland WL, Summers SA
    Obesity and dyslipidemia are risk factors for metabolic disorders including diabetes and cardiovascular disease. Sphingolipids such as ceramide and glucosylceramides, while being a relatively minor component of the lipid mileu in most tissues, may be amongst the most pathogenic lipids in the onset of the sequelae associated with excess adiposity. Circulating factors associated with obesity (e.g. saturated fatty acids, inflammatory cytokines) selectively induce enzymes which promote sphingolipid synthesis, and lipidomic profiling reveals relationships between tissue sphingolipid levels and certain metabolic diseases. Moreover, studies in cultured cells and isolated tissues implicate sphingolipids in certain cellular events associated with diabetes and car...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1418221</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1418221</guid>        </item>
        <item>
            <title>Role of Hormones, Genes and Environment in Human Cryptorchidism.</title>
            <link>http://www.medworm.com/index.php?rid=1401139&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436703%26dopt%3DAbstract</link>
            <description>Authors: Foresta C, Zuccarello D, Garolla A, Ferlin A
    Cryptorchidism is the most frequent congenital birth defect in male children (2-4% in full-term male births) and it has the potential to impact the health of the human male. In fact, although it is often considered a mild malformation, it represents the best characterized risk factor for reduced fertility and testicular cancer. Furthermore, some reports have highlighted a significant increase in the prevalence of cryptorchidism over the last few decades. Etiology of cryptorchidism remains for the most part unknown, and cryptorchidism itself might be considered a complex disease. Major regulators of testicular descent from intra-abdominal location into the bottom of the scrotum are the Leydig-cell derived hormones testosterone and In...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401139</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401139</guid>        </item>
        <item>
            <title>Advances in Male Contraception.</title>
            <link>http://www.medworm.com/index.php?rid=1401138&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436704%26dopt%3DAbstract</link>
            <description>Authors: Page ST, Amory JK, Bremner WJ
    Despite significant advances in contraceptive options for women over the last 50 years, world population continues to grow rapidly. Scientists and activists alike point to the devastating environmental impacts that population pressures have caused including global warming from the developed world and hunger and disease in less developed areas. Moreover, almost of half of all pregnancies are still unwanted or unplanned. Clearly, there is a need for expanded, reversible, contraceptive options. Multicultural surveys demonstrate men's willingness to participate in contraception and their female partners to trust them to do so. Notwithstanding their paucity of options, male methods including vasectomy and condoms account for almost a third of contracep...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401138</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401138</guid>        </item>
        <item>
            <title>The Unfolded Protein Response: A Pathway That Links Insulin Demand with {beta}-Cell Failure and Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=1401137&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436705%26dopt%3DAbstract</link>
            <description>Authors: Scheuner D, Kaufman RJ
    The endoplasmic reticulum (ER) is the entry site into the secretory pathway for newly synthesized proteins destined for the cell surface or released into the extracellular milieu. The study of protein folding and trafficking within the ER is an extremely active area of research that has provided novel insights into many disease processes. Cells have evolved mechanisms to modulate the capacity and quality of the ER protein-folding machinery to prevent the accumulation of unfolded or misfolded proteins. These signaling pathways, collectively termed the unfolded protein response (UPR), detect the accumulation of unfolded and misfolded proteins in the ER lumen through three ER transmembrane sensors, IRE1alpha, PERK, and ATF6. The UPR sensors signal a transcr...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401137</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401137</guid>        </item>
        <item>
            <title>Growth Hormone, Insulin-Like Growth Factors, and the Skeleton.</title>
            <link>http://www.medworm.com/index.php?rid=1401136&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436706%26dopt%3DAbstract</link>
            <description>Authors: Giustina A, Mazziotti G, Canalis E
    Growth Hormone (GH) and insulin-like growth factor-I (IGF-I) are important regulators of bone homeostasis and are central to the achievement of normal longitudinal bone growth and bone mass. Although GH may act directly on skeletal cells, most of its effects are mediated by IGF-I, which is present in the systemic circulation and is synthesized by peripheral tissues. The availability of IGF-I is regulated by IGF binding proteins. IGF-I enhances the differentiated function of the osteoblast and bone formation. Adult GH deficiency causes low bone turnover osteoporosis with high risk of vertebral and non-vertebral fractures, and the low bone mass can be partially reversed by GH replacement. Acromegaly is characterized by high bone turnover, which...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401136</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401136</guid>        </item>
        <item>
            <title>Neonatal Diabetes Mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=1401135&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436707%26dopt%3DAbstract</link>
            <description>Authors: Aguilar-Bryan L, Bryan J
    An explosion of work over the last decade has produced insight into the multiple hereditary causes of a nonimmunologic form of diabetes diagnosed most frequently within the first 6 months of life. These studies are providing increased understanding of genes involved in the entire chain of steps that control glucose homeostasis. Neonatal diabetes is now understood to arise from mutations in genes that play critical roles in the development of the pancreas, of beta-cell apoptosis and insulin processing, as well as the regulation of insulin release. For the basic researcher this work is providing novel tools to explore fundamental molecular and cellular processes. For the clinician, these studies underscore the need to identify the genetic cause underlyin...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401135</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401135</guid>        </item>
        <item>
            <title>Monogenic Diabetes in the Young, Pharmacogenetics and Relevance to Multifactorial Forms of Type 2 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=1401134&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436708%26dopt%3DAbstract</link>
            <description>Authors: Vaxillaire M, Froguel P
    Most valuable breakthroughs in the genetics of type 2 diabetes for the past two decades have arisen from candidate gene studies and familial linkage analysis of maturity-onset diabetes of the young (MODY), an autosomal dominant form of diabetes typically occurring before 25 years of age caused by primary insulin secretion defects. Despite its low prevalence, MODY is not a single entity but presents genetic, metabolic and clinical heterogeneity. MODY can result from mutations in at least 6 different genes encoding the glucose sensor enzyme glucokinase and transcription factors which participate in a regulatory network essential for adult b-cell function. Additional genes have been described in other discrete phenotypes or syndromic forms of diabetes. Whe...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401134</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401134</guid>        </item>
        <item>
            <title>Cognitive Dysfunction and Diabetes Mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=1401133&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18436709%26dopt%3DAbstract</link>
            <description>Authors: Kodl CT, Seaquist ER
    The deleterious effects of diabetes mellitus on the retinal, renal, cardiovascular, and peripheral nervous systems are widely acknowledged. Less attention has been given to the effect of diabetes on cognitive function. Both type 1 and type 2 diabetes mellitus have been associated with reduced performance on numerous domains of cognitive function. The exact pathophysiology of cognitive dysfunction in diabetes is not completely understood, but it is likely that hyperglycemia, vascular disease, hypoglycemia, and insulin resistance play significant roles. Modalities to study the effect of diabetes on the brain have evolved over the years, including neurocognitive testing, evoked response potentials, and magnetic resonance imaging. Although much insightful rese...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1401133</comments>
            <pubDate>Thu, 24 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1401133</guid>        </item>
        <item>
            <title>Islet Amyloid in Type 2 Diabetes, and the Toxic Oligomer Hypothesis.</title>
            <link>http://www.medworm.com/index.php?rid=1277352&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18314421%26dopt%3DAbstract</link>
            <description>Authors: Haataja L, Gurlo T, Huang CJ, Butler PC
    Type 2 diabetes (T2DM) is characterized by insulin resistance, defective insulin secretion, loss of beta-cell mass with increased beta-cell apoptosis and islet amyloid. The islet amyloid is derived from islet amyloid polypeptide (IAPP, amylin), a protein coexpressed and cosecreted with insulin by pancreatic beta-cells. In common with other amyloidogenic proteins, IAPP has the propensity to form membrane permeant toxic oligomers. Accumulating evidence suggests that these toxic oligomers, rather than the extracellular amyloid form of these proteins, are responsible for loss of neurons in neurodegenerative diseases. In this review, we discuss emerging evidence to suggest that formation of intracellular IAPP oligomers may contribute to beta-...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1277352</comments>
            <pubDate>Tue, 26 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1277352</guid>        </item>
        <item>
            <title>Functions of Normal and Malignant Prostatic Stem/Progenitor Cells in Tissue Regeneration and Cancer Progression and Novel Targeting Therapies.</title>
            <link>http://www.medworm.com/index.php?rid=1251519&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18292464%26dopt%3DAbstract</link>
            <description>Authors: Mimeault M, Mehta PP, Hauke R, Batra SK
    This review summarizes the recent advancements that have improved our understanding of the functions of prostatic stem/progenitor cells in maintaining homeostasis of the prostate gland. We also describe the oncogenic events that may contribute to their malignant transformation into prostatic cancer stem/progenitor cells during cancer initiation and progression to metastatic disease stages. The molecular mechanisms that may contribute to the intrinsic or the acquisition of a resistant phenotype by the prostatic cancer stem/progenitor cells and their differentiated progenies with a luminal phenotype to the current therapies and disease relapse are also reviewed. The emphasis is on the critical functions of distinct tumorigenic signaling ca...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1251519</comments>
            <pubDate>Thu, 21 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1251519</guid>        </item>
        <item>
            <title>Targeting {beta}-Cell Mass in Type 2 Diabetes: Promise and Limitations of New Drugs Based on Incretins.</title>
            <link>http://www.medworm.com/index.php?rid=1251518&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18292465%26dopt%3DAbstract</link>
            <description>Authors: Salehi M, Aulinger BA, D'Alessio DA
    Progressive inherent insulin secretory defects, due to either functional abnormalities of the pancreatic beta-cells or a reduction in beta-cell mass are the cornerstone of type 2 diabetes. Incretin-based drugs hold the potential to improve glucose tolerance by immediate favorable effect on beta-cell physiology as well as by expanding or at least maintaining beta-cell mass, which may delay the progression of the disease. Long-term studies in humans are needed to elaborate on this effect.
    PMID: 18292465 [PubMed - as supplied by publisher] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1251518</comments>
            <pubDate>Thu, 21 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1251518</guid>        </item>
        <item>
            <title>A Lifetime of Aldosterone Excess: Long-Term Consequences of Altered Regulation of Aldosterone Production for Cardiovascular Function.</title>
            <link>http://www.medworm.com/index.php?rid=1251517&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18292466%26dopt%3DAbstract</link>
            <description>Authors: Connell JM, Mackenzie SM, Freel EM, Fraser R, Davies E
    Up to 15% of patients with essential hypertension have inappropriate regulation of aldosterone; although only a minority have distinct adrenal tumors, recent evidence shows that mineralocorticoid receptor activation contributes to the age-related blood pressure rise and illustrates the importance of aldosterone in determining cardiovascular risk. Aldosterone also has a major role in progression and outcome of ischaemic heart disease. These data highlight the need to understand better the regulation of aldosterone synthesis and its action. Aldosterone effects are mediated mainly through classical nuclear receptors that alter gene transcription. In classic epithelial target tissues, signalling mechanisms are relatively well ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1251517</comments>
            <pubDate>Thu, 21 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1251517</guid>        </item>
        <item>
            <title>Syndromes of Ketosis-Prone Diabetes Mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=1251516&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18292467%26dopt%3DAbstract</link>
            <description>Authors: Balasubramanyam A, Nalini R, Hampe CS, Maldonado M
    Ketosis-prone diabetes (KPD) is a widespread, emerging, heterogeneous syndrome, characterized by patients who present with diabetic ketoacidosis or unprovoked ketosis but who do not necessarily have the typical phenotype of autoimmune type 1 diabetes. Multiple, severe forms of beta-cell dysfunction appear to underlie the pathophysiology of KPD. Until recently, the syndrome has lacked an accurate, clinically relevant, and etiologically useful classification scheme. We have utilized a large, longitudinally followed, heterogeneous, multiethnic cohort of KPD patients to identify four clinically and pathophysiologically distinct subgroups that are separable by the presence or absence of beta-cell autoimmunity and the presence or ab...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1251516</comments>
            <pubDate>Thu, 21 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1251516</guid>        </item>
        <item>
            <title>Cellular Signaling by Fibroblast Growth Factors (FGFs) and Their Receptors (FGFRs) in Male Reproduction.</title>
            <link>http://www.medworm.com/index.php?rid=1177262&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18216218%26dopt%3DAbstract</link>
            <description>Authors: Cotton LM, O'Bryan MK, Hinton BT
    The major function of the reproductive system is to ensure the survival of the species by passing on hereditary traits from one generation to the next. This is accomplished through the production of gametes and the generation of hormones which function in the maturation and regulation of the reproductive system. It is well established that normal development and function of the male reproductive system is mediated by endocrine and paracrine signaling pathways. Fibroblast growth factors (FGFs), their receptors (FGFRs) and signaling cascades have been implicated in a diverse range of cellular processes including: proliferation, apoptosis, cell survival, chemotaxis, cell adhesion, motility, and differentiation. The maintenance and regulation of co...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1177262</comments>
            <pubDate>Wed, 23 Jan 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1177262</guid>        </item>
        <item>
            <title>Cross-Talk between the Estrogen Receptor and the HER Tyrosine Kinase Receptor Family: Molecular Mechanism and Clinical Implications for Endocrine Therapy Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=1177261&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18216219%26dopt%3DAbstract</link>
            <description>Authors: Arpino G, Wiechmann L, Osborne CK, Schiff R
    Breast cancer evolution and tumor progression are governed by the complex interactions between steroid receptor [estrogen receptor (ER) and progesterone receptor (PgR)] and growth factor receptor signaling. In recent years, the field of cancer therapy has witnessed the emergence of multiple strategies targeting these specific cancer pathways and key molecules (ER and growth factor receptors) to arrest tumor growth and achieve tumor eradication; treatment success, however, has varied and both de novo (upfront) and acquired resistance have proven a challenge. Recent studies of ER biology have revealed new insights into ER action in breast cancer and have highlighted the role of an intimate cross-talk between the ER and HER family signa...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1177261</comments>
            <pubDate>Wed, 23 Jan 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1177261</guid>        </item>
        <item>
            <title>The Role of Membrane Glycoprotein PC-1/ENPP1 in the Pathogenesis of Insulin Resistance and Related Abnormalities.</title>
            <link>http://www.medworm.com/index.php?rid=1160704&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18199690%26dopt%3DAbstract</link>
            <description>Authors: Goldfine ID, Maddux BA, Youngren JF, Reaven G, Accili D, Trischitta V, Vigneri R, Frittitta L
    Insulin resistance is a major feature of most patients with type 2 diabetes mellitus (T2D). A number of laboratories have observed that membrane glycoprotein PC-1 (ENNP1) is either overexpressed or overactive in muscle, adipose tissue, fibroblasts, and other tissues of insulin-resistant individuals, both nondiabetic and diabetic. Moreover, in cultured cells in vitro and in transgenic mice in vivo, PC-1 overexpression impairs insulin stimulation of insulin receptor (IR) activation and downstream signaling. PC-1 binds to the connecting domain of the IR alpha-subunit that is located in residues 485-599. The connecting domain transmits insulin binding in the alpha-subunit to activation of...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1160704</comments>
            <pubDate>Wed, 16 Jan 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1160704</guid>        </item>
        <item>
            <title>What Can We Learn from Rodents about Prolactin in Humans?</title>
            <link>http://www.medworm.com/index.php?rid=1078949&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18057139%26dopt%3DAbstract</link>
            <description>The objective of this review is to compare and contrast multiple aspects of PRL, from structure to regulation, and from physiology to pathology in rats, mice, and humans. At each juncture, questions are raised whether, or to what extent, data from rodents are relevant to PRL homeostasis in humans. Most current knowledge on PRL has been obtained from studies with rats, and more recently, from the use of transgenic mice. Although this information is indispensable for understanding PRL in human health and disease, there is sufficient disparity in the control of the production, distribution and physiological functions of PRL among these species to warrant careful and judicial extrapolation to humans.
    PMID: 18057139 [PubMed - as supplied by publisher] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1078949</comments>
            <pubDate>Wed, 05 Dec 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1078949</guid>        </item>
        <item>
            <title>RANKL and OPG Regulation of Bone Remodeling in Health and Disease.</title>
            <link>http://www.medworm.com/index.php?rid=1078948&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18057140%26dopt%3DAbstract</link>
            <description>Authors: Kearns AE, Khosla S, Kostenuik P
    Osteoclasts and osteoblasts dictate skeletal mass, structure, and strength via their respective roles in resorbing and forming bone. Bone remodeling is a spatially coordinated lifelong process whereby old bone is removed by osteoclasts and replaced by bone-forming osteoblasts. The refilling of resorption cavities is incomplete in many pathologic states, which leads to a net loss of bone mass with each remodeling cycle. Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling, which leads to accelerated bone loss and increased risk of fracture. Bone resorption is dependent on a cytokine known as RANKL (receptor activator of nuclear factor kappa B ligand), a TNF (tumor necrosis factor) family membe...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1078948</comments>
            <pubDate>Wed, 05 Dec 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1078948</guid>        </item>
        <item>
            <title>Cytokines and {beta}-Cell Biology: from Concept to Clinical Translation.</title>
            <link>http://www.medworm.com/index.php?rid=1064048&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18048762%26dopt%3DAbstract</link>
            <description>Authors: Donath MY, St&amp;#xF8;rling J, Berchtold LA, Billestrup N, Mandrup-Poulsen T
    The tale of cytokines and the beta-cell is a long story, starting with in vitro discovery in 1984, evolving via descriptive and phenomenological studies to detailed mapping of the signalling pathways, gene- and protein expression patterns, molecular and biochemical effector mechanisms to in vivo studies in spontaneously diabetic and transgenic animal models. Only very recently have steps been taken to translate the accumulating compelling preclinical data into clinical trials. The aim of this chapter is to present an overview of early and recent key observations from our own groups as well as other laboratories that serve to illuminate the road from concept to clinical translation.
    PMID: 18048762 [Pu...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1064048</comments>
            <pubDate>Thu, 29 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1064048</guid>        </item>
        <item>
            <title>Glucolipotoxicity: Fuel Excess and {beta}-Cell Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=1064047&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18048763%26dopt%3DAbstract</link>
            <description>Authors: Poitout V, Robertson RP
    Glucotoxicity, lipotoxicity, and glucolipotoxicity are secondary phenomena that are proposed to play a role in all forms of type 2 diabetes. The underlying concept is that once the primary pathogenesis of diabetes is established, probably involving both genetic and environmental forces, hyperglycemia and very commonly hyperlipidemia ensue and thereafter exert additional damaging or toxic effects on the beta-cell. In addition to their contribution to the deterioration of beta-cell function after the onset of the disease, elevations of plasma fatty acid levels that often accompany insulin resistance may, as glucose levels begin to rise outside of the normal range, also play a pathogenic role in the early stages of the disease. Because hyperglycemia is a p...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1064047</comments>
            <pubDate>Thu, 29 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1064047</guid>        </item>
        <item>
            <title>The Role for Endoplasmic Reticulum Stress in Diabetes Mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=1064046&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18048764%26dopt%3DAbstract</link>
            <description>Authors: Eizirik DL, Cardozo AK, Cnop M
    Accumulating evidence suggests that endoplasmic reticulum (ER) stress plays a role in the pathogenesis of diabetes, contributing to pancreatic beta-cell loss and insulin resistance. Components of the unfolded protein response (UPR) play a dual role in beta-cells, acting as beneficial regulators under physiological conditions or as triggers of beta-cell dysfunction and apoptosis under situations of chronic stress. Novel findings suggest that &quot;what makes a beta-cell a beta-cell&quot;, i.e., its enormous capacity to synthesize and secrete insulin, is also its &quot;Achilles heel&quot;, rendering it vulnerable to chronic high glucose and fatty acid exposure, agents that contribute to beta-cell failure in type 2 diabetes. In this review, we address the transition fr...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1064046</comments>
            <pubDate>Thu, 29 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1064046</guid>        </item>
        <item>
            <title>The Clinical Significance of Subclinical Thyroid Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=1018744&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17991805%26dopt%3DAbstract</link>
            <description>Authors: Biondi B, Cooper DS
    Subclinical thyroid disease (SCTD) is defined as serum FT4 and FT3 levels within their respective reference ranges in the presence of abnormal serum thyrotropin-stimulating hormone levels. Subclinical thyroid disease is being diagnosed more frequently in clinical practice in young and middle-aged people as well as in the elderly. However, the clinical significance of subclinical thyroid dysfunction is much debated. Subclinical hyper- and hypothyroidism can have repercussions on the cardiovascular system and bone, as well as on other organs and systems. However, the treatment and management of SCTD and population screening are controversial despite the potential risk of progression to overt disease, and there is no consensus on the thyroid hormone and thyrot...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1018744</comments>
            <pubDate>Thu, 08 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1018744</guid>        </item>
        <item>
            <title>Adiposity, the Metabolic Syndrome, and Breast Cancer in African-American and White American Women.</title>
            <link>http://www.medworm.com/index.php?rid=1008983&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981890%26dopt%3DAbstract</link>
            <description>Authors: Rose DP, Haffner SM, Baillargeon J
    Breast cancer, the second most common cause of cancer-related deaths in American women, varies substantially in incidence and mortality according to race and ethnicity in the United States. Although the overall incidence of breast cancer among African-American (AA) women is lower than in white American women, this cancer is more common in young premenopausal AA women, and AA breast cancer patients of all ages are more likely to have advanced disease at diagnosis, higher risk of recurrence, and poorer overall prognosis. Epidemiological studies indicate that these differences may be attributable in part to variation in obesity and body fat distribution. Additionally, AA women more frequently exhibit breast cancer with an aggressive and metastat...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1008983</comments>
            <pubDate>Fri, 02 Nov 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1008983</guid>        </item>
        <item>
            <title>Androgen Receptor (AR) Coregulators: A Diversity of Functions Converging on and Regulating the AR Transcriptional Complex.</title>
            <link>http://www.medworm.com/index.php?rid=961305&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17940184%26dopt%3DAbstract</link>
            <description>Authors: Heemers HV, Tindall DJ
    Androgens, acting through the androgen receptor (AR), are responsible for the development of the male phenotype during embryogenesis, the achievement of sexual maturation at puberty and the maintenance of male reproductive function and behavior in adulthood. In addition, androgens affect a wide variety of nonreproductive tissues. Moreover, aberrant androgen action plays a critical role in multiple pathologies, including prostate cancer and androgen insensitivity syndromes. The formation of a productive AR transcriptional complex requires the functional and structural interaction of the AR with its coregulators. In the last decade, an overwhelming and ever increasing number of proteins have been proposed to possess AR coactivating or corepressing characte...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=961305</comments>
            <pubDate>Tue, 16 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">961305</guid>        </item>
        <item>
            <title>BRAF Mutation in Papillary Thyroid Cancer: Pathogenic Role, Molecular Bases, and Clinical Implications.</title>
            <link>http://www.medworm.com/index.php?rid=961304&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17940185%26dopt%3DAbstract</link>
            <description>Authors: Xing M
    In recent years, the T1799A BRAF mutation in thyroid cancer has received enthusiastic investigation, and significant progress has been made toward understanding its tumorigenic role and clinical significance. Among various thyroid tumors, this mutation occurs uniquely in papillary thyroid cancer (PTC), the most common endocrine malignancy, and some apparently PTC-derived anaplastic thyroid cancers. Many studies have found this mutation to be associated with those clinicopathological characteristics of PTC that are conventionally known to predict tumor progression and recurrence, including, for example, old patient age, extrathyroidal invasion, lymph node metastasis, and advanced tumor stages. Direct association of BRAF mutation with the clinical progression, recurrence,...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=961304</comments>
            <pubDate>Tue, 16 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">961304</guid>        </item>
        <item>
            <title>Extranuclear Steroid Receptors: Nature and Actions.</title>
            <link>http://www.medworm.com/index.php?rid=932366&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17916740%26dopt%3DAbstract</link>
            <description>Authors: Hammes SR, Levin ER
    Rapid effects of steroid hormones result from the actions of specific receptors localized most often to the plasma membrane. Fast-acting membrane-initiated steroid signaling (MISS)(1) leads to the modification of existing proteins and cell behaviors. Rapid steroid-triggered signaling through calcium, amine release, and kinase activation also impacts the regulation of gene expression by steroids, sometimes requiring integration with nuclear steroid receptor function. In this and other ways, the integration of all steroid actions in the cell coordinates outcomes such as cell fate, proliferation, differentiation, and migration. The nature of the receptors is of intense interest, and significant data suggest that extranuclear and nuclear steroid receptor pools ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=932366</comments>
            <pubDate>Thu, 04 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">932366</guid>        </item>
        <item>
            <title>Uteroglobin: A Steroid-Inducible Immunomodulatory Protein That Founded the Secretoglobin Superfamily.</title>
            <link>http://www.medworm.com/index.php?rid=932365&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17916741%26dopt%3DAbstract</link>
            <description>Authors: Mukherjee AB, Zhang Z, Chilton BS
    Blastokinin or uteroglobin (UG) is a steroid-inducible, evolutionarily conserved, secreted protein that has been extensively studied from the standpoint of its structure and molecular biology. However, the physiological function(s) of UG still remains elusive. Isolated from the uterus of rabbits during early pregnancy, UG is the founding member of a growing superfamily of proteins called Secretoglobin (Scgb). Numerous studies demonstrated that UG is a multifunctional protein with anti-inflammatory/ immunomodulatory properties. It inhibits soluble phospholipase A2 activity, binds and perhaps sequesters hydrophobic ligands such as progesterone, retinols, polychlorinated biphenyls, phospholipids and prostaglandins. In addition to its anti-inflamm...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=932365</comments>
            <pubDate>Thu, 04 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">932365</guid>        </item>
        <item>
            <title>An Illustrated Review of Early Pancreas Development in the Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=890555&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17881611%26dopt%3DAbstract</link>
            <description>Authors: J&amp;#xF8;rgensen MC, Ahnfelt-R&amp;#xF8;nne J, Hald J, Madsen OD, Serup P, Hecksher-S&amp;#xF8;rensen J
    Pancreas morphogenesis and cell differentiation is highly conserved among vertebrates during fetal development. The pancreas develops through simple bud-like structures on the primitive gut tube to a highly branched organ containing many specialized cell types. This review presents an overview of key molecular components and important signaling sources illustrated by an extensive three dimensional (3D) imaging of the developing mouse pancreas at single cell resolution. The 3D documentation covers the time window between e8.5 and e14.5 in which all the pancreatic cell types become specified and therefore includes gene expression patterns of pancreatic endocrine hormones, exocrine gene ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=890555</comments>
            <pubDate>Wed, 19 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">890555</guid>        </item>
        <item>
            <title>SNAREing Kv and KATP channels: Tuning {beta}-Cell Excitability with Syntaxin-1A and Other Exocytotic Proteins.</title>
            <link>http://www.medworm.com/index.php?rid=887607&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17878408%26dopt%3DAbstract</link>
            <description>Authors: Leung YM, Kwan EP, Ng B, Kang Y, Gaisano HY
    The three SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) proteins, syntaxin, SNAP25 (synaptosome-associated protein of 25 kDa) and synaptobrevin, constitute the minimal machinery for exocytosis in secretory cells such as neurons and neuroendocrine cells by forming a series of complexes prior to and during vesicle fusion. It was subsequently found that these SNARE proteins not only participate in vesicle fusion, but also tether with voltage-dependent Ca(2+) channels (VDCC) to form an excitosome that precisely regulates calcium entry at the site of exocytosis. In pancreatic islet beta-cells, ATP-sensitive K(+) (KATP) channel closure by high ATP concentration leads to membrane depolarization, VDCC opening...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=887607</comments>
            <pubDate>Tue, 18 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">887607</guid>        </item>
        <item>
            <title>Neuropeptide Y Receptors Selective Ligands in the Treatment of Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=845379&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17785427%26dopt%3DAbstract</link>
            <description>Authors: Mm K, A I
    Obesity is a serious public health problem throughout the world, affecting both developed societies and developing countries. The central nervous system has developed a meticulously interconnected circuitry in order to keep us fed and in adequate nutritional state. One of these consequences is that an energy dense environment favors the development of obesity NPY is one of the most abundant and widely distributed peptides in the central nervous system (CNS) of both rodents and humans and has been implicated in a variety of physiological actions. Within the hypothalamus, NPY play an essential role in the control of food intake and body weight. Centrally administered NPY causes robust increases in food intake and body weight and, with chronic administration, can eventu...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=845379</comments>
            <pubDate>Tue, 04 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">845379</guid>        </item>
        <item>
            <title>Immunologic Responses to Exogenous Insulin.</title>
            <link>http://www.medworm.com/index.php?rid=845378&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17785428%26dopt%3DAbstract</link>
            <description>Authors: Fineberg SE, Kawabata TT, Finco-Kent D, Fountaine RJ, Finch GL, Krasner AS
    Regardless of purity and origin, therapeutic insulins continue to be immunogenic in humans. However, severe immunologic complications occur rarely, and less severe events affect a small minority of patients. Insulin antibodies (IAs) may be detectable in insulin-na&amp;#xEF;ve individuals who have a high likelihood of developing type 1 diabetes or in patients who have had viral disorders, have been treated with various drugs, or have autoimmune disorders or paraneoplastic syndromes. This suggests that under certain circumstances immune tolerance to insulin can be overcome. Factors that can lead to more or less susceptibility to humoral responses to exogenous insulin include the recipient's immune response ge...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=845378</comments>
            <pubDate>Tue, 04 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">845378</guid>        </item>
        <item>
            <title>The Growth Hormone/Insulin-like Growth Factor-I Axis in Exercise and Sport.</title>
            <link>http://www.medworm.com/index.php?rid=845377&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17785429%26dopt%3DAbstract</link>
            <description>Authors: Gibney J, Healy ML, S&amp;#xF6;nksen PH
    The syndrome of adult growth hormone (GH) deficiency (AGHD) and the effects of GH replacement therapy provide a useful model with which to study the effects of the GH/insulin-like growth factor-I (IGF-I) axis on exercise physiology. Measures of exercise performance including maximal oxygen uptake (VO2max) and ventilatory threshold (VeT) are impaired in AGHD and improved by GH replacement, probably through some combination of increased oxygen delivery to exercising muscle, increased fatty acid availability with glycogen sparing, increased muscle strength, improved body composition and improved thermoregulation. In normal subjects, in addition to the long-term effects of GH/IGF-I status, there is evidence that the acute GH response to exercise...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=845377</comments>
            <pubDate>Tue, 04 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">845377</guid>        </item>
        <item>
            <title>The Endocrine Society Laureate Awards.</title>
            <link>http://www.medworm.com/index.php?rid=829533&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17722365%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 17722365 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=829533</comments>
            <pubDate>Wed, 01 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">829533</guid>        </item>
        <item>
            <title>The Endocrine Society 2007 Laureate Awards.</title>
            <link>http://www.medworm.com/index.php?rid=829532&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17722366%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 17722366 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=829532</comments>
            <pubDate>Wed, 01 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">829532</guid>        </item>
        <item>
            <title>The complex role of estrogens in inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=748283&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17640948%26dopt%3DAbstract</link>
            <description>Authors: Straub RH
    There is still the unresolved paradox with respect to the immunomodulating role of estrogens: On one side, we recognize inhibition of bone resorption and suppression of inflammation in several animal models of chronic inflammatory diseases. On the other hand, we realize the immunosupportive role of estrogens in trauma/sepsis and the proinflammatory effects in some chronic autoimmune diseases in humans. This review examines possible causes for this paradox. This review delineates that effects of estrogens dependent on criteria such as 1) the immune stimulus (foreign antigens or autoantigens) and subsequent antigen-specific immune responses (e.g., T cell inhibited by estrogens versus activation of B cell), 2) the cell types involved during different phases of the disea...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=748283</comments>
            <pubDate>Thu, 19 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">748283</guid>        </item>
        <item>
            <title>Nuclear Receptor Coregulators and Human Disease.</title>
            <link>http://www.medworm.com/index.php?rid=715888&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17609497%26dopt%3DAbstract</link>
            <description>Authors: Lonard DM, Lanz RB, O'malley BW
    Nuclear receptor (NR) coregulators (coactivators and corepressors) are essential elements in regulating nuclear receptor-mediated transcription. In a little more than a decade since their discovery, these proteins have been studied mechanistically and reveal that the regulation of transcription is a highly controlled and complex process. Because of their central role in regulating NR-mediated transcription and in coordinating intercompartmental metabolic processes, disruptions in coregulator biology can lead to pathological states. To date, the extent to which they are involved in human disease has not been widely appreciated. In a complete literature survey, we have identified nearly 300 distinct coregulators, revealing that a great variety of ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=715888</comments>
            <pubDate>Tue, 03 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">715888</guid>        </item>
        <item>
            <title>Cardiovascular Actions of Insulin.</title>
            <link>http://www.medworm.com/index.php?rid=635582&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17525361%26dopt%3DAbstract</link>
            <description>Authors: Muniyappa R, Montagnani M, Koh KK, Quon MJ
    Insulin has important vascular actions to stimulate production of nitric oxide (NO) from endothelium. This leads to capillary recruitment, vasodilation, increased blood flow, and subsequent augmentation of glucose disposal in classical insulin target tissues (e.g, skeletal muscle). Phosphatidylinositol 3-kinase (PI3K)-dependent insulin signaling pathways regulating endothelial production of NO share striking parallels with metabolic insulin signaling pathways. Distinct MAP-kinase-dependent insulin signaling pathways (largely unrelated to metabolic actions of insulin) regulate secretion of the vasoconstrictor endothelin-1 from endothelium. These and other cardiovascular actions of insulin contribute to coupling metabolic and hemodynami...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=635582</comments>
            <pubDate>Thu, 24 May 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">635582</guid>        </item>
        <item>
            <title>Role of chemokines in endocrine autoimmune diseases.</title>
            <link>http://www.medworm.com/index.php?rid=590551&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17475924%26dopt%3DAbstract</link>
            <description>This article reviews the recent literature including basic science, animal models and clinical studies, regarding the role of these chemokines in autoimmune endocrine diseases. The potential clinical applications of assaying the serum levels of CXCL10 and the value of such measurements are reviewed. Clinical studies addressing the issue of a role for serum CXCL10 measurement in Graves'disease, Graves'ophthalmopathy, chronic autoimmune thyroiditis, Type 1 diabetes mellitus and Addison's disease, have been considered. The principal aim was to propose that chemokines, and in particular CXCL10, should be no more considered as belonging exclusively to basic science, but rather should be used for providing new insights in the clinical management of patients with endocrine autoimmune diseases.
  ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=590551</comments>
            <pubDate>Wed, 02 May 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">590551</guid>        </item>
        <item>
            <title>Gonadotropins and ovarian cancer.</title>
            <link>http://www.medworm.com/index.php?rid=576867&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17463396%26dopt%3DAbstract</link>
            <description>Authors: Choi JH, Wong AS, Huang HF, Leung PC
    Ovarian epithelial cancer (OEC) accounts for 90% of all ovarian cancers and is the leading cause of death from gynecological cancers in North America and Europe. Despite its clinical significance, the factors that regulate the development and progression of ovarian cancer are among the least understood of all major human malignancies. The two gonadotropins, follicle stimulating hormone and luteinizing hormone, are key regulators of ovarian cell functions and the potential role of gonadotropins in the pathogenesis of ovarian cancer is suggested. Ovarian carcinomas have been found to express specific receptors for gonadotropins. The presence of gonadotropins in ovarian tumor fluid suggests the importance of these factors in the transformation...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=576867</comments>
            <pubDate>Thu, 26 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">576867</guid>        </item>
        <item>
            <title>Novel perspectives for progesterone in HRT, with special reference to the nervous system.</title>
            <link>http://www.medworm.com/index.php?rid=544951&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17431228%26dopt%3DAbstract</link>
            <description>Authors: Schumacher M, Guennoun R, Ghoumari A, Massaad C, Robert F, El-Etr M, Akwa Y, Rajkowski K, Baulieu EE
    The utility and safety of postmenopausal hormone replacement therapy (HRT) has recently been put into question by large clinical trials. Their outcome has been extensively commented upon, but discussions have mainly been limited to the effects of estrogens. In fact, progestagens are generally only considered with respect to their usefulness in preventing estrogen stimulation of uterine hyperplasia and malignancy. In addition, various risks have been attributed to progestagens, and their omission from HRT has been considered, but this may be to underestimate their potential benefits and therapeutic promises. A major reason for the controversial reputation of progestagens is that...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=544951</comments>
            <pubDate>Thu, 12 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">544951</guid>        </item>
        <item>
            <title>Hepatic TNF signaling and NF-{kappa}B: effects on liver homeostasis and beyond.</title>
            <link>http://www.medworm.com/index.php?rid=544944&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17431229%26dopt%3DAbstract</link>
            <description>Authors: Wullaert A, van Loo G, Heyninck K, Beyaert R
    The pro-inflammatory cytokine TNF has a pivotal role in liver pathophysiology, since it holds the capacity to induce both hepatocyte cell death and hepatocyte proliferation. This dual effect of TNF on hepatocytes reflects its ability to induce both NF-kappaB dependent gene expression and cell death. Multiple studies have demonstrated the crucial role of the transcription factor NF-kappaB in the decision between life and death of a hepatocyte. Massive hepatocyte apoptosis preceding embryonic lethality in NF-kappaB-deficient mice constituted the first indication of an essential anti-apoptotic function of NF-kappaB in the liver. Although many studies confirmed this crucial cytoprotective role of NF-kappaB in adult liver, a number of ge...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=544944</comments>
            <pubDate>Thu, 12 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">544944</guid>        </item>
        <item>
            <title>Notch signaling in development and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=526187&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17409286%26dopt%3DAbstract</link>
            <description>Authors: Bolós V, Grego-Bessa J, de la Pompa JL
    Notch is an evolutionarily conserved local cell signaling mechanism that participates in a variety of cellular processes: cell fate specification, differentiation, proliferation, apoptosis, adhesion, epithelial-mesenchymal transition, migration and angiogenesis. These processes can be subverted in Notch-mediated pathological situations. In the first part of this review, we will discuss the role of Notch in vertebrate central nervous system development, somitogenesis, cardiovascular and endocrine development, with attention to the mechanisms by which Notch regulates cell fate specification and patterning in these tissues. In the second part, we will review the molecular aspects of Notch-mediated neoplasias, where Notch can act as an oncog...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=526187</comments>
            <pubDate>Wed, 04 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">526187</guid>        </item>
        <item>
            <title>Tumor Cell-Organ Microenvironment Interactions in the Pathogenesis of Cancer Metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=526186&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17409287%26dopt%3DAbstract</link>
            <description>Authors: Langley RR, Fidler IJ
    The process of cancer metastasis is sequential and selective and contains stochastic elements. The growth of metastases represents the endpoint of many lethal events that few tumor cells can survive. Primary tumors consist of multiple subpopulations of cells with heterogeneous metastatic properties, and the outcome of metastasis depends on the interplay of tumor cells with various host factors. The findings that different metastases can originate from different progenitor cells account for the biological diversity that exists among various metastases. Even within a solitary metastasis of proven clonal origin, however, heterogeneity of biological characteristics can develop rapidly. The pathogenesis of metastasis depends on multiple interactions of metasta...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=526186</comments>
            <pubDate>Wed, 04 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">526186</guid>        </item>
        <item>
            <title>The Role of {alpha}-Cell Dysregulation in Fasting and Postprandial Hyperglycemia in Type 2 Diabetes and Therapeutic Implications.</title>
            <link>http://www.medworm.com/index.php?rid=526185&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17409288%26dopt%3DAbstract</link>
            <description>This article begins with a brief overview of the discovery of glucagon and the contributions that somatostatin and a sensitive and selective assay for pancreatic (vs gut) glucagon made to understanding the physiologic and pathophysiologic roles of glucagon. Studies utilizing these tools to establish the function of glucagon in normal nutrient homeostasis and to document a relative glucagon excess in type 2 diabetes mellitus (T2DM) and precursors thereof are then discussed. The evidence that glucagon excess contributes to the development and maintenance of fasting hyperglycemia and that failure to suppress glucagon secretion contributes to postprandial hyperglycemia is then reviewed. Although key human studies are emphasized, salient animal studies highlighting the importance of glucagon in...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=526185</comments>
            <pubDate>Wed, 04 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">526185</guid>        </item>
        <item>
            <title>{beta}-Cell Failure in Diabetes and Preservation by Clinical Treatment.</title>
            <link>http://www.medworm.com/index.php?rid=499171&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17353295%26dopt%3DAbstract</link>
            <description>Authors: Wajchenberg BL
    There is a progressive deterioration in beta-cell function and mass in type 2 diabetics. It was found that islet function was about 50% of normal at the time of diagnosis, and a reduction in beta-cell mass of about 60% was shown at necropsy. The reduction of beta-cell mass is attributable to accelerated apoptosis. The major factors for progressive loss of beta-cell function and mass are glucotoxicity, lipotoxicity, proinflammatory cytokines, leptin, and islet cell amyloid. Impaired beta-cell function and possibly beta-cell mass appear to be reversible, particularly at early stages of the disease where the limiting threshold for reversibility of decreased beta-cell mass has probably not been passed. Among the interventions to preserve or &quot;rejuvenate&quot; beta-cells, ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=499171</comments>
            <pubDate>Thu, 22 Mar 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">499171</guid>        </item>
        <item>
            <title>Perspectives and limitations of microarray based gene expression profiling of thyroid tumors.</title>
            <link>http://www.medworm.com/index.php?rid=474792&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17353294%26dopt%3DAbstract</link>
            <description>Authors: Eszlinger M, Krohn K, Kukulska A, Jarzab B, Paschke R
    Microarray technology has become a powerful tool to analyze the gene expression of tens of thousands of genes simultaneously. Microarray based gene expression profiles are available for malignant thyroid tumors (i.e. follicular thyroid carcinoma, and papillary thyroid carcinoma), and for benign thyroid tumors (such as autonomously functioning thyroid nodules, and cold thyroid nodules). In general, the two main foci of microarray investigations are improved understanding of the pathophysiology / molecular etiology of thyroid neoplasia and the detection of genetic markers that could improve the differential diagnosis of thyroid tumors. Their results revealed new features, not known from one gene studies. Simultaneously, the i...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=474792</comments>
            <pubDate>Mon, 12 Mar 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">474792</guid>        </item>
        <item>
            <title>Beta-cell failure in diabetes and preservation by clinical treatment.</title>
            <link>http://www.medworm.com/index.php?rid=474791&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17353295%26dopt%3DAbstract</link>
            <description>BETA-CELL FAILURE IN DIABETES AND PRESERVATION BY CLINICAL TREATMENT.
    Endocr Rev. 2007 Mar 12;
    Authors: Wajchenberg BL
    There is a progressive deterioration in beta-cell function and mass in type 2 diabetics. It was found that islet function was about 50% of normal at the time of diagnosis, and a reduction in beta-cell mass of about 60% was shown at necropsy. The reduction of beta-cell mass is attributable to accelerated apoptosis. The major factors for progressive loss of beta-cell function and mass are glucotoxicity, lipotoxicity, proinflammatory cytokines, leptin, and islet cell amyloid. Impaired beta-cell function and possibly beta-cell mass appear to be reversible, particularly at early stages of the disease where the limiting threshold for reversibility of decreased beta-c...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=474791</comments>
            <pubDate>Mon, 12 Mar 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">474791</guid>        </item>
        <item>
            <title>Pituitary Tumor Transforming Gene: Physiology and Implications for Tumorigenesis.</title>
            <link>http://www.medworm.com/index.php?rid=438105&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17325339%26dopt%3DAbstract</link>
            <description>Authors: Vlotides G, Eigler T, Melmed S
    Pituitary tumor transforming gene-1 (PTTG1) is over-expressed in a variety of endocrine-related tumors, especially pituitary, thyroid, breast, ovarian and uterine tumors, as well as non-endocrine related cancers, involving the CNS, pulmonary, and gastrointestinal system. Forced PTTG1 expression induces cell transformation in vitro and tumor formation in nude mice. In some tumors, high PTTG1 levels correlate with invasiveness, and PTTG1 has been identified as a key signature gene associated with tumor metastasis. Increasing evidence supports a multi-functional role of PTTG1 in cell physiology and tumorigenesis. Physiologic PTTG1 properties include securin activity, DNA damage/repair regulation and involvement in organ development and metabolism. T...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=438105</comments>
            <pubDate>Mon, 26 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">438105</guid>        </item>
        <item>
            <title>Small for gestational age: short stature and beyond.</title>
            <link>http://www.medworm.com/index.php?rid=438114&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17322454%26dopt%3DAbstract</link>
            <description>Authors: Saenger P, Czernichow P, Hughes I, Reiter EO
    Depending on the definitions used, up to 10% of all live-born neonates are small for gestational age (SGA). Although the vast majority of these children show catch-up growth by 2 years of age, 1 in 10 do not. It is increasingly recognized that those who are born SGA are at risk of developing metabolic disease later in life. Reduced fetal growth has been shown to be associated with an increased risk of insulin resistance, obesity, cardiovascular disease and type 2 diabetes mellitus. The majority of pathology is seen in adults who show spontaneous catch-up growth as children. There is evidence to suggest that some of the metabolic consequences of intrauterine growth retardation in children born SGA can be mitigated by ensuring early a...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=438114</comments>
            <pubDate>Fri, 23 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">438114</guid>        </item>
        <item>
            <title>Roles of epidermal growth factor family in the regulation of postnatal somatic growth.</title>
            <link>http://www.medworm.com/index.php?rid=438112&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17322455%26dopt%3DAbstract</link>
            <description>Authors: Xian CJ
    Ligands of the epidermal growth factor receptor (EGF-R), known important for supporting tissue development particularly in the gut and brain, have also been implicated in regulating postnatal somatic growth. Although optimal levels of both milk-borne and endogenous EGF-R ligands are important for supporting postnatal somatic growth through regulating gastrointestinal growth and maturation, supra-physiological levels of EGF-R ligands can cause retarded and disproportionate growth and alter body composition as they can increase growth of epithelial tissues but decrease masses of muscle, fat, and bone. Apart from their indirect roles in influencing growth possibly via regulating levels of insulin-like growth factor (IGF-I) and its binding proteins (IGFBPs), EGF-R ligands ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=438112</comments>
            <pubDate>Fri, 23 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">438112</guid>        </item>
        <item>
            <title>Alpha-cells of the endocrine pancreas: 35 years of research but the enigma remains.</title>
            <link>http://www.medworm.com/index.php?rid=430102&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17261637%26dopt%3DAbstract</link>
            <description>Authors: Gromada J, Franklin I, Wollheim CB
    Glucagon, a hormone secreted from the alpha-cells of the endocrine pancreas, is critical for blood glucose homeostasis. It is the major counterpart to insulin and is released during hypoglycemia to induce hepatic glucose output. The control of glucagon secretion is multifactorial and involves direct effects of nutrients on alpha-cell stimulus-secretion coupling as well as paracrine regulation by insulin and zinc and other factors secreted from neighboring beta- and delta-cells within the islet of Langerhans. Glucagon secretion is also regulated by circulating hormones and the autonomic nervous system. In this review, we describe the components of the alpha-cell stimulus secretion coupling and how nutrient metabolism in the alpha-cell leads to...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=430102</comments>
            <pubDate>Thu, 01 Feb 2007 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">430102</guid>        </item>
        <item>
            <title>{alpha}-Cells of the Endocrine Pancreas: 35 Years of Research but the Enigma Remains.</title>
            <link>http://www.medworm.com/index.php?rid=390295&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17261637%26dopt%3DAbstract</link>
            <description>Authors: Gromada J, Franklin I, Wollheim CB
    Glucagon, a hormone secreted from the alpha-cells of the endocrine pancreas, is critical for blood glucose homeostasis. It is the major counterpart to insulin and is released during hypoglycemia to induce hepatic glucose output. The control of glucagon secretion is multifactorial and involves direct effects of nutrients on alpha-cell stimulus-secretion coupling as well as paracrine regulation by insulin and zinc and other factors secreted from neighboring beta- and delta-cells within the islet of Langerhans. Glucagon secretion is also regulated by circulating hormones and the autonomic nervous system. In this review, we describe the components of the alpha-cell stimulus secretion coupling and how nutrient metabolism in the alpha-cell leads to...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=390295</comments>
            <pubDate>Mon, 29 Jan 2007 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">390295</guid>        </item>
        <item>
            <title>INSIGHTS INTO MATERIAL AND STRUCTURAL BASIS OF BONE FRAGILITY FROM DISEASES ASSOCIATED WITH FRACTURES. How determinants of the biomechanical properties of bone are compromised by disease.</title>
            <link>http://www.medworm.com/index.php?rid=340238&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17200084%26dopt%3DAbstract</link>
            <description>Authors: Chavassieux P, Seeman E, Delmas PD
    Minimal trauma fractures in bone diseases are the result of bone fragility. Rather than considering bone fragility as being the result of a reduced amount of bone, we recognize that bone fragility is the result of changes in the material and structural properties of bone. A better understanding of the contribution of each component of the material composition and structure, and how these interact to maintain whole bone strength is obtained by the study of metabolic bone diseases. Disorders of collagen (osteogenesis imperfecta and Paget's disease of bone), of mineral content, composition and distribution (fluorosis and osteomalacia), disease of high remodelling (postmenopausal osteoporosis, hyperparathyroidism, hyperthyroidism, low remodelling...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=340238</comments>
            <pubDate>Thu, 04 Jan 2007 15:43:02 +0100</pubDate>
            <guid isPermaLink="false">340238</guid>        </item>
        <item>
            <title>In memoriam: jack gorski (1931-2006).</title>
            <link>http://www.medworm.com/index.php?rid=321768&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17167123%26dopt%3DAbstract</link>
            <description>Authors: Katzenellenbogen BS
    
    PMID: 17167123 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=321768</comments>
            <pubDate>Sat, 16 Dec 2006 02:22:01 +0100</pubDate>
            <guid isPermaLink="false">321768</guid>        </item>
        <item>
            <title>Editorial: obesity research--can discovery outpace the epidemic?</title>
            <link>http://www.medworm.com/index.php?rid=321767&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17167124%26dopt%3DAbstract</link>
            <description>Authors: Moore DD, Kahn BB
    
    PMID: 17167124 [PubMed - in process] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=321767</comments>
            <pubDate>Sat, 16 Dec 2006 02:22:01 +0100</pubDate>
            <guid isPermaLink="false">321767</guid>        </item>
        <item>
            <title>Emerging Therapeutic Strategies for Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=289524&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17122357%26dopt%3DAbstract</link>
            <description>Authors: Foster-Schubert KE, Cummings DE
    The rising tide of obesity is one of the most pressing health issues of our time, yet existing medicines to combat the problem are disappointingly limited in number and effectiveness. Fortunately, a recent burgeoning of mechanistic insights into the neuroendocrine regulation of body weight provides an expanding list of molecular targets for novel, rationally designed anti-obesity pharmaceuticals. In this review, we articulate a set of conceptual principles that we feel could help prioritize among these molecules in the development of obesity therapeutics, based on an understanding of energy homeostasis. We focus primarily on central targets, highlighting selected strategies to stimulate endogenous catabolic signals or inhibit anabolic signals. E...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=289524</comments>
            <pubDate>Sun, 26 Nov 2006 05:30:02 +0100</pubDate>
            <guid isPermaLink="false">289524</guid>        </item>
        <item>
            <title>Genetics of Obesity in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=289523&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17122358%26dopt%3DAbstract</link>
            <description>Authors: Farooqi IS, O'rahilly S
    Considerable attention has focused on deciphering the hypothalamic pathways that mediate the behavioral and metabolic effects of leptin. We and others have identified several single gene defects that disrupt the molecules in the leptin-melanocortin pathway causing severe obesity in humans. In this review, we consider these human monogenic obesity syndromes and discuss how far the characterization of these patients has informed our understanding of the physiological role of leptin and the melanocortins in the regulation of human body weight and neuroendocrine function.
    PMID: 17122358 [PubMed - as supplied by publisher] (Source: ENDOCR REV)</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=289523</comments>
            <pubDate>Sun, 26 Nov 2006 05:30:02 +0100</pubDate>
            <guid isPermaLink="false">289523</guid>        </item>
        <item>
            <title>Understanding and Addressing the Epidemic of Obesity: An Energy Balance Perspective.</title>
            <link>http://www.medworm.com/index.php?rid=289522&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17122359%26dopt%3DAbstract</link>
            <description>Authors: Hill JO
    The intent of this paper is to address the obesity epidemic which is a term used to describe the sudden and rapid increase in obesity rates that began in the 1980s and continue unabated today. Since 1980, the entire population, regardless of starting weight, is gradually gaining weight. This has led to escalating obesity rates and to obesity being considered one of the most serious public health challenges facing the world. At one level, the obesity epidemic is a classic gene-environment interaction where the human genotype is susceptible to environmental influences that affect energy intake and energy expenditure. It is also a problem of energy balance. Understanding the etiology of obesity requires the study of how behavioral and environmental factors have interacted...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=289522</comments>
            <pubDate>Sun, 26 Nov 2006 05:30:02 +0100</pubDate>
            <guid isPermaLink="false">289522</guid>        </item>
        <item>
            <title>Complex actions of sex steroids in adipose tissue, the cardiovascular system, and brain: Insights from basic science and clinical studies.</title>
            <link>http://www.medworm.com/index.php?rid=276002&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16763155%26dopt%3DAbstract</link>
            <description>Authors: Turgeon JL, Carr MC, Maki PM, Mendelsohn ME, Wise PM
    Recent publications describing the results of the Women's Health Initiative (WHI) and other studies reporting the impact of hormone therapy on aging women have spurred reexamination of the broad use of estrogens and progestins during the postmenopausal years. Here, we review the complex pharmacology of these hormones, the diverse and sometimes opposite effects that result from the use of different estrogenic and progestinic compounds, given via different delivery routes in different concentrations and treatment sequence, and to women of different ages and health status. We examine our new and growing appreciation of the role of estrogens in the immune system and the inflammatory response, and we pose the concept that estroge...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=276002</comments>
            <pubDate>Wed, 15 Nov 2006 19:27:03 +0100</pubDate>
            <guid isPermaLink="false">276002</guid>        </item>
        <item>
            <title>Expanding the scales: The multiple roles of MCH in regulating energy balance and other biological functions.</title>
            <link>http://www.medworm.com/index.php?rid=276001&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16788162%26dopt%3DAbstract</link>
            <description>Authors: Pissios P, Bradley RL, Maratos-Flier E
    Melanin-concentrating hormone (MCH) is a cyclic peptide originally identified as a 17-amino-acid circulating hormone in teleost fish, where it is secreted by the pituitary in response to stress and environmental stimuli. In fish, MCH lightens skin color by stimulating aggregation of melanosomes, pigment-containing granules in melanophores, cells of neuroectodermal origin found in fish scales. Although the peptide structure between fish and mammals is highly conserved, in mammals, MCH has no demonstrable effects on pigmentation; instead, based on a series of pharmacological and genetic experiments, MCH has emerged as a critical hypothalamic regulator of energy homeostasis, having effects on both feeding behavior and energy expenditure.
   ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=276001</comments>
            <pubDate>Wed, 15 Nov 2006 19:27:03 +0100</pubDate>
            <guid isPermaLink="false">276001</guid>        </item>
        <item>
            <title>The role of voltage-gated calcium channels in pancreatic beta-cell physiology and pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=276000&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16868246%26dopt%3DAbstract</link>
            <description>Authors: Yang SN, Berggren PO
    Voltage-gated calcium (CaV) channels are ubiquitously expressed in various cell types throughout the body. In principle, the molecular identity, biophysical profile, and pharmacological property of CaV channels are independent of the cell type where they reside, whereas these channels execute unique functions in different cell types, such as muscle contraction, neurotransmitter release, and hormone secretion. At least six CaValpha1 subunits, including CaV1.2, CaV1.3, CaV2.1, CaV2.2, CaV2.3, and CaV3.1, have been identified in pancreatic beta-cells. These pore-forming subunits complex with certain auxiliary subunits to conduct L-, P/Q-, N-, R-, and T-type CaV currents, respectively. beta-Cell CaV channels take center stage in insulin secretion and play an i...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=276000</comments>
            <pubDate>Wed, 15 Nov 2006 19:27:03 +0100</pubDate>
            <guid isPermaLink="false">276000</guid>        </item>
        <item>
            <title>Studies on the Physiologic Functions of the Melanocortin System.</title>
            <link>http://www.medworm.com/index.php?rid=261368&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17077189%26dopt%3DAbstract</link>
            <description>Authors: Cone RD
    The melanocortin system refers to a set of hormonal, neuropeptidergic, and paracrine signaling pathways that are defined by components that include the five G protein-coupled melanocortin receptors, peptide agonists derived from the proopiomelanoocortin preprohormone precursor, and the endogenous antagonists, agouti and agouti-related protein. This signaling system regulates a remarkably diverse array of physiological functions including pigmentation, adrenocortical steroidogenesis, energy homeostasis, natriuresis, erectile responses, energy homeostasis, and exocrine gland secretion. There are many complex and unique aspects of melanocortin signaling, such as the existence of endogenous antagonists, the agouti proteins, that act at three of the five melanocortin recept...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=261368</comments>
            <pubDate>Fri, 03 Nov 2006 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">261368</guid>        </item>
        <item>
            <title>Gut peptides in the regulation of food intake and energy homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=261367&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17077190%26dopt%3DAbstract</link>
            <description>Authors: Murphy KG, Dhillo WS, Bloom SR
    Gut hormones signal to the central nervous system to influence energy homeostasis. Evidence supports the existence of a system in the gut that senses the presence of food in the gastrointestinal tract and signals to the brain via neural and endocrine mechanisms to regulate short-term appetite and satiety. Recent evidence has shown that specific gut hormones administered at physiological or pathophysiological concentrations can influence appetite in rodents and humans. Gut hormones therefore have an important physiological role in post-prandial satiety, and gut hormone signaling systems represent important pharmaceutical targets for potential anti-obesity therapies. Our laboratory investigates the role of gut hormones in energy homeostasis and has...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=261367</comments>
            <pubDate>Fri, 03 Nov 2006 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">261367</guid>        </item>
        <item>
            <title>The Molecular Control of Corpus Luteum Formation, Function and Regression.</title>
            <link>http://www.medworm.com/index.php?rid=261366&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17077191%26dopt%3DAbstract</link>
            <description>Authors: Stocco C, Telleria C, Gibori G
    The corpus luteum (CL) is one of the few endocrine glands that forms from the remains of another organ and whose function and survival are limited in scope and time. The CL is the site of rapid remodeling, growth, differentiation and death of cells originating from granulosa, theca, capillaries, and fibroblasts. The apparent raison d'etre of the CL is the production of progesterone and all the structural and functional features of this gland are geared toward this end. Because of its unique importance for successful pregnancies, the mammals have evolved a complex series of check and balances that maintains progesterone at appropriate levels throughout gestation. The formation, maintenance, regression, and steroidogenesis of the CL are among the m...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=261366</comments>
            <pubDate>Fri, 03 Nov 2006 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">261366</guid>        </item>
        <item>
            <title>Adipose Tissue-Derived Factors: Impact on Health and Disease.</title>
            <link>http://www.medworm.com/index.php?rid=249257&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17056740%26dopt%3DAbstract</link>
            <description>Authors: Trujillo ME, Scherer PE
    The endocrine functions of the adipose organ are widely studied at this stage. The adipose organ, and in particular adipocytes, communicate with almost all other organs. While some adipose tissue pads assume the functions as distinct &quot;miniorgans,&quot; adipocytes can also be present in smaller numbers interspersed with other cell types (1). While fat pads have the potential to have a significant systemic impact, adipocytes may also affect neighboring tissues through paracrine interactions. These local or systemic effects are mediated through lipid and protein factors. The protein factors are commonly referred as adipokines. Their expression and post-translational modifications can undergo dramatic changes under different metabolic conditions. Due to the fact...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=249257</comments>
            <pubDate>Thu, 26 Oct 2006 03:02:02 +0100</pubDate>
            <guid isPermaLink="false">249257</guid>        </item>
        <item>
            <title>Jekyll and hyde: two faces of cannabinoid signaling in male and female fertility.</title>
            <link>http://www.medworm.com/index.php?rid=240394&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682502%26dopt%3DAbstract</link>
            <description>Authors: Wang H, Dey SK, Maccarrone M
    Mammalian reproduction is a complicated process designed to diversify and strengthen the genetic complement of the offspring and to safeguard regulatory systems at various steps for propagating procreation. An emerging concept in mammalian reproduction is the role of endocannabinoids, a group of endogenously produced lipid mediators, that bind to and activate cannabinoid receptors. Although adverse effects of cannabinoids on fertility have been implicated for years, the mechanisms by which they exert these effects were not clearly understood. With the identification of cannabinoid receptors, endocannabinoid ligands, their key synthetic and hydrolytic pathways, and the generation of mouse models missing cannabinoid receptors, a wealth of information...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=240394</comments>
            <pubDate>Thu, 19 Oct 2006 05:40:02 +0100</pubDate>
            <guid isPermaLink="false">240394</guid>        </item>
        <item>
            <title>Role of adipose tissue as an inflammatory organ in human diseases.</title>
            <link>http://www.medworm.com/index.php?rid=240393&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16684901%26dopt%3DAbstract</link>
            <description>Authors: Schäffler A, Müller-Ladner U, Schölmerich J, Büchler C
    Reviews on the inflammatory role of adipose tissue outside the field of metabolism are rare. There is increasing evidence provided by numerous basic research studies from nearly all internal medicine subspecializations that adipocytes and adipocytokines are involved in primary inflammatory processes and diseases. Therefore, it is the aim of the present review to discuss and to summarize the current knowledge on the inflammatory role of adipocytokines and special types of regional adipocytes such as retroorbital, synovial, visceral, subdermal, peritoneal, and bone marrow adipocytes in internal medicine diseases. Future clinical and therapeutic implications are discussed.
    PMID: 16684901 [PubMed - indexed for MEDLINE]...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=240393</comments>
            <pubDate>Thu, 19 Oct 2006 05:40:02 +0100</pubDate>
            <guid isPermaLink="false">240393</guid>        </item>
        <item>
            <title>Advances in the treatment of prolactinomas.</title>
            <link>http://www.medworm.com/index.php?rid=240392&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16705142%26dopt%3DAbstract</link>
            <description>Authors: Gillam MP, Molitch ME, Lombardi G, Colao A
    Prolactinomas account for approximately 40% of all pituitary adenomas and are an important cause of hypogonadism and infertility. The ultimate goal of therapy for prolactinomas is restoration or achievement of eugonadism through the normalization of hyperprolactinemia and control of tumor mass. Medical therapy with dopamine agonists is highly effective in the majority of cases and represents the mainstay of therapy. Recent data indicating successful withdrawal of these agents in a subset of patients challenge the previously held concept that medical therapy is a lifelong requirement. Complicated situations, such as those encountered in resistance to dopamine agonists, pregnancy, and giant or malignant prolactinomas, may require multim...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=240392</comments>
            <pubDate>Thu, 19 Oct 2006 05:40:02 +0100</pubDate>
            <guid isPermaLink="false">240392</guid>        </item>
        <item>
            <title>Germ cell tumors in the intersex gonad: old paths, new directions, moving frontiers.</title>
            <link>http://www.medworm.com/index.php?rid=240391&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16735607%26dopt%3DAbstract</link>
            <description>This article reviews the recent literature regarding the prevalence of germ cell tumors in patients with DSD. Some major limitations regarding this topic, including a confusing terminology referring to the different forms of intersex disorders and unclear criteria for the diagnosis of malignant germ cells at an early age (maturation delay vs. early steps in malignant transformation) are discussed. Thereafter, an overview of the recent advances that have been made in our knowledge of germ cell tumor development and the correct diagnosis of early neoplastic lesions in this patient population is provided. A new classification system for patients with DSD is proposed as a tool to refine our insight in the prevalence of germ cell tumors in specific diagnostic groups.
    PMID: 16735607 [PubMed ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=240391</comments>
            <pubDate>Thu, 19 Oct 2006 05:40:02 +0100</pubDate>
            <guid isPermaLink="false">240391</guid>        </item>
        <item>
            <title>PGC-1 coactivators, energy homeostasis, and metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=221694&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17018837%26dopt%3DAbstract</link>
            <description>Authors: Handschin C, Spiegelman BM
    Many biological programs are regulated at the transcriptional level. This is generally achieved by the concerted actions of several transcription factors. Recent findings have shown that, in many cases, transcriptional coactivators coordinate the overall regulation of the biological programs. One of the best-studied examples of coactivator control of metabolic pathways is the peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1) family. These proteins are strong activators of mitochondrial function and are thus dominant regulators of oxidative metabolism in a variety of tissues. The PGC-1 coactivators themselves are subject to powerful regulation at the transcriptional and post-translational level. Recent studies have elucidated the ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=221694</comments>
            <pubDate>Thu, 05 Oct 2006 14:29:02 +0100</pubDate>
            <guid isPermaLink="false">221694</guid>        </item>
        <item>
            <title>The Genetic Landscape of Type 2 Diabetes in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=221693&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17018838%26dopt%3DAbstract</link>
            <description>Authors: Clee SM, Attie AD
    Inbred mouse strains provide genetic diversity comparable to that of the human population. Like humans, mice have a wide range of diabetes-related phenotypes. The inbred mouse strains differ in the response of their critical physiological functions, such as insulin sensitivity, insulin secretion, beta-cell proliferation and survival, and fuel partitioning, to diet and obesity. Most of the critical genes underlying these differences have not been identified, even though many loci have been mapped. The dramatic improvements in genomic and bioinformatics resources are accelerating the pace of gene discovery. This review describes how mouse genetics can be used to discover diabetes-related genes, summarizes how the mouse strains in differ in their diabetes-relate...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=221693</comments>
            <pubDate>Thu, 05 Oct 2006 14:29:02 +0100</pubDate>
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        <item>
            <title>Membrane initiated actions of estrogens in neuroendocrinology: emerging principles.</title>
            <link>http://www.medworm.com/index.php?rid=221692&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17018839%26dopt%3DAbstract</link>
            <description>MEMBRANE INITIATED ACTIONS OF ESTROGENS IN NEUROENDOCRINOLOGY: EMERGING PRINCIPLES.
    Endocr Rev. 2006 Oct 3;
    Authors: Vasudevan N, Pfaff DW
    Hormonal ligands for the nuclear receptor superfamily have at least two interacting mechanisms of action: a) classical transcriptional regulation of target genes (genomic mechanisms); and b) non-genomic actions, which are initiated at the cell membrane, which could impact transcription. Though transcriptional mechanisms are increasingly well understood, membrane-initiated actions of these ligands are incompletely understood. Historically, this has led to a considerable divergence of thought in the molecular endocrine field. We have attempted to uncover principles of hormone action that are relevant to membrane-initiated actions of estrogens....</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=221692</comments>
            <pubDate>Thu, 05 Oct 2006 14:29:02 +0100</pubDate>
            <guid isPermaLink="false">221692</guid>        </item>
        <item>
            <title>The role of the IGF system in cancer growth and metastasis: overview and recent insights.</title>
            <link>http://www.medworm.com/index.php?rid=158825&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16931767%26dopt%3DAbstract</link>
            <description>Authors: Samani AA, Yakar S, Leroith D, Brodt P
    IGF-I receptor signaling and functions are mediated through the activities of a complex molecular network of positive (e.g. the type of insulin like growth factor, IGF-I) and negative (e.g. the type II insulin like growth factor receptor, IGF-IIR) effectors. Under normal physiological conditions, the balance between the expression and activities of these molecules is tightly controlled. Changes in this delicate balance (e.g. overexpression of one effector) may trigger a cascade of molecular events that can ultimately lead to malignancy. In recent years, evidence has been mounting that the IGF axis may be involved in human cancer progression and can be targeted for therapeutic intervention. Here we review old and more recent evidence on th...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=158825</comments>
            <pubDate>Thu, 24 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">158825</guid>        </item>
        <item>
            <title>The Hair Follicle as an Estrogen Target and Source.</title>
            <link>http://www.medworm.com/index.php?rid=133084&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16877675%26dopt%3DAbstract</link>
            <description>Authors: Ohnemus U, Uenalan M, Inzunza J, Gustafsson JA, Paus R
    For many decades, androgens have dominated endocrine research in hair growth control, and androgen metabolism or the androgen receptor currently are the key targets for systemic, pharmacological hair growth control in clinical medicine. However, it has long been known that estrogens also profoundly alter hair follicle growth and cycling by binding to locally expressed high affinity estrogen receptors (ERs). Besides altering the transcription of genes with estrogen-responsive elements, 17beta-estradiol (E2) also modifies androgen metabolism within distinct subunits of the pilosebaceous unit (i.e. hair follicle and sebaceous gland). The latter displays prominent aromatase activity, the key enzyme for androgen conversion to E...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=133084</comments>
            <pubDate>Fri, 28 Jul 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">133084</guid>        </item>
        <item>
            <title>The Role of Voltage-Gated Calcium Channels in Pancreatic {beta}-Cell Physiology and Pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=125369&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16868246%26dopt%3DAbstract</link>
            <description>Authors: Yang SN, Berggren PO
    Voltage-gated calcium (CaV) channels are ubiquitously expressed in various cell types throughout the body. In principle, the molecular identity, biophysical profile and pharmacological property of CaV channels are independent of the cell type where they reside, whereas these channels execute unique functions in different cell types, such as muscle contraction, neurotransmitter release and hormone secretion. At least six CaValpha1 subunits including CaV1.2, CaV1.3, CaV2.1, CaV2.2, CaV2.3, and CaV3.1 have been identified in pancreatic beta-cells. These pore-forming subunits complex with certain auxiliary subunits to conduct L-, P/Q-, N-, R-, and T-type CaV currents, respectively. beta-Cell CaV channels take center stage in insulin secretion and play an impor...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=125369</comments>
            <pubDate>Tue, 25 Jul 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">125369</guid>        </item>
        <item>
            <title>RET as a diagnostic and therapeutic target in sporadic and hereditary endocrine tumors.</title>
            <link>http://www.medworm.com/index.php?rid=118229&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16849421%26dopt%3DAbstract</link>
            <description>Authors: de Groot JW, Links TP, Plukker JT, Lips CJ, Hofstra RM
    The RET gene encodes a receptor tyrosine kinase which is expressed in neural crest derived cell lineages. The RET receptor plays a crucial role in regulating cell proliferation, migration, differentiation and survival through embryogenesis. Activating mutations in RET lead to the development of several inherited and non-inherited diseases. Germline point mutations are found in the cancer sydromes multiple endocrine neoplasia type 2 (MEN 2), including MEN 2A and 2B, and familial medullary thyroid carcinoma (FMTC). These syndromes are autosomal dominantly inherited. The identification of mutations associated with these syndromes has led to genetic testing to identify patients at risk for MEN 2 and FMTC and subsequent impleme...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=118229</comments>
            <pubDate>Tue, 18 Jul 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">118229</guid>        </item>
        <item>
            <title>Craniopharyngiomas.</title>
            <link>http://www.medworm.com/index.php?rid=168449&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16543382%26dopt%3DAbstract</link>
            <description>Authors: Karavitaki N, Cudlip S, Adams CB, Wass JA
    Craniopharyngiomas are rare, mainly sellar/parasellar, epithelial tumors diagnosed during childhood or adult life. Histologically, two primary subtypes have been recognized (adamantinomatous and papillary) with an as yet, unclarified pathogenesis. They may present with a variety of manifestations (neurological, visual, and hypothalamo-pituitary). Despite their benign histological appearance, they often show an unpredictable growth pattern, which, combined with the lack of randomized studies, poses significant difficulties in the establishment of an optimal therapeutic protocol. This should focus on the prevention of recurrence(s), improvement of survival, reduction of the significant disease and treatment-related morbidity (endocrine, ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=168449</comments>
            <pubDate>Wed, 14 Jun 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">168449</guid>        </item>
        <item>
            <title>Genetic analysis of chromosome pairing, recombination, and cell cycle control during first meiotic prophase in mammals.</title>
            <link>http://www.medworm.com/index.php?rid=168448&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16543383%26dopt%3DAbstract</link>
            <description>Authors: Cohen PE, Pollack SE, Pollard JW
    Meiosis is a double-division process that is preceded by only one DNA replication event to produce haploid gametes. The defining event in meiosis is prophase I, during which chromosome pairs locate each other, become physically connected, and exchange genetic information. Although many aspects of this process have been elucidated in lower organisms, there has been scant information available until now about the process in mammals. Recent advances in genetic analysis, especially in mice and humans, have revealed many genes that play essential roles in meiosis in mammals. These include cell cycle-regulatory proteins that couple the exit from the premeiotic DNA synthesis to the progression through prophase I, the chromosome structural proteins inv...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=168448</comments>
            <pubDate>Wed, 14 Jun 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">168448</guid>        </item>
        <item>
            <title>Endocrine regulation of HOX genes.</title>
            <link>http://www.medworm.com/index.php?rid=168447&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16632680%26dopt%3DAbstract</link>
            <description>Authors: Daftary GS, Taylor HS
    Hox genes have a well-characterized role in embryonic development, where they determine identity along the anteroposterior body axis. Hox genes are expressed not only during embryogenesis but also in the adult, where they are necessary for functional differentiation. Despite the known function of these genes as transcription factors, few regulatory mechanisms that drive Hox expression are known. Recently, several hormones and their cognate receptors have been shown to regulate Hox gene expression and thereby mediate development in the embryo as well as functional differentiation in the adult organism. Estradiol, progesterone, testosterone, retinoic acid, and vitamin D have been shown to regulate Hox gene expression. In the embryo, the endocrine system dir...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=168447</comments>
            <pubDate>Wed, 14 Jun 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">168447</guid>        </item>
        <item>
            <title>Molecular control of cell cycle progression in the pancreatic beta-cell.</title>
            <link>http://www.medworm.com/index.php?rid=168446&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16638909%26dopt%3DAbstract</link>
            <description>Authors: Cozar-Castellano I, Fiaschi-Taesch N, Bigatel TA, Takane KK, Garcia-Ocaña A, Vasavada R, Stewart AF
    Type 1 and type 2 diabetes both result from inadequate production of insulin by the beta-cells of the pancreatic islet. Accordingly, strategies that lead to increased pancreatic beta-cell mass, as well as retained or enhanced function of islets, would be desirable for the treatment of diabetes. Although pancreatic beta-cells have long been viewed as terminally differentiated and irreversibly arrested, evidence now indicates that beta-cells can and do replicate, that this replication can be enhanced by a variety of maneuvers, and that beta-cell replication plays a quantitatively significant role in maintaining pancreatic beta-cell mass and function. Because beta-cells have been ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=168446</comments>
            <pubDate>Wed, 14 Jun 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">168446</guid>        </item>
        <item>
            <title>The roles of specific genes implicated as circulating factors involved in normal and disordered phosphate homeostasis: frizzled related protein-4, matrix extracellular phosphoglycoprotein, and fibroblast growth factor 23.</title>
            <link>http://www.medworm.com/index.php?rid=108658&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16467171%26dopt%3DAbstract</link>
            <description>Authors: White KE, Larsson TE, Econs MJ
    Normal serum phosphate (Pi) concentrations are relatively tightly controlled by endocrine mediators of Pi balance. Recent data involving several disorders of Pi homeostasis have shed new light on the regulation of serum Pi balance. It has been hypothesized that circulating phosphaturic factors, or phosphatonins, exist that, when present at high serum concentrations, directly act on the kidney to induce renal Pi wasting. This review will focus upon recently discovered factors that are overexpressed in tumors associated with tumor-induced osteomalacia and have reported activity consistent with effecting Pi balance in vivo. Currently, the best-characterized group of phosphatonin-like polypeptides includes secreted frizzled related protein-4, matrix ...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=108658</comments>
            <pubDate>Sun, 14 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">108658</guid>        </item>
        <item>
            <title>The molecular mechanisms underlying the regulation of the biological activity of corticotropin-releasing hormone receptors: implications for physiology and pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=108657&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16484629%26dopt%3DAbstract</link>
            <description>Authors: Hillhouse EW, Grammatopoulos DK
    The CRH receptor (CRH-R) is a member of the secretin family of G protein-coupled receptors. Wide expression of CRH-Rs in the central nervous system and periphery ensures that their cognate agonists, the family of CRH-like peptides, are capable of exerting a wide spectrum of actions that underpin their critical role in integrating the stress response and coordinating the activity of fundamental physiological functions, such as the regulation of the cardiovascular system, energy balance, and homeostasis. Two types of mammal CRH-R exist, CRH-R1 and CRH-R2, each with unique splicing patterns and remarkably distinct pharmacological properties, but similar signaling properties, probably reflecting their distinct and sometimes contrasting biological fu...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=108657</comments>
            <pubDate>Sun, 14 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">108657</guid>        </item>
        <item>
            <title>Insulin resistance and atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=108656&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16492903%26dopt%3DAbstract</link>
            <description>Authors: Nigro J, Osman N, Dart AM, Little PJ
    The epidemic of obesity in the developed world over the last two decades is driving a large increase in type 2 diabetes and consequentially setting the scene for an impending wave of cardiovascular morbidity and mortality. It is only now being recognized that the major antecedent of type 2 diabetes, insulin resistance with its attendant syndrome, is the major underlying cause of the susceptibility to type 2 diabetes and cardiovascular disease. In metabolic tissues, insulin signaling via the phosphatidylinositol-3-kinase pathway leads to glucose uptake so that in insulin resistance a state of hyperglycemia occurs; other factors such as dyslipidemia and hypertension also arise. In cardiovascular tissues there are two pathways of insulin recep...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=108656</comments>
            <pubDate>Sun, 14 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">108656</guid>        </item>
        <item>
            <title>The influence of growth hormone status on physical impairments, functional limitations, and health-related quality of life in adults.</title>
            <link>http://www.medworm.com/index.php?rid=108655&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16543384%26dopt%3DAbstract</link>
            <description>Authors: Woodhouse LJ, Mukherjee A, Shalet SM, Ezzat S
    The availability of recombinant human GH and somatostatin analogs has resulted in widespread treatment for adults with GH deficiency (GHD) and those with GH excess (acromegaly). Despite being at opposite ends of the spectrum in terms of their GH/IGF-I axis, both of these populations experience overlapping somatic impairments. Adults with untreated GHD have low circulating levels of IGF-I that manifest as altered body composition with increased fat and reduced lean body and skeletal muscle mass. At the other end of the spectrum, adults with GH excess, who have elevated levels of IGF-I, also have altered body composition. Impairments that result from disorders of either GHD or GH excess are both associated with increased functional l...</description>
            <author>ENDOCR REV</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=108655</comments>
            <pubDate>Sun, 14 May 2006 06:00:00 +0100</pubDate>
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        <item>
            <title>Roles of skeletal muscle and peroxisome proliferator-activated receptors in the development and treatment of obesity.</title>
            <link>http://www.medworm.com/index.php?rid=108654&amp;cid=s_33004_15_f&amp;fid=33004&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16556851%26dopt%3DAbstract</link>
            <description>Authors: López-Soriano J, Chiellini C, Maffei M, Grimaldi PA, Argilés JM
    Metabolic disturbances associated with alterations in lipid metabolism, such as obesity, type 2 diabetes, and syndrome X, are becoming more and more prominent in Western societies. Despite extensive research in such pathologies and their molecular basis, we are still far from completely understanding how these metabolic perturbations are produced and interrelate and, consequently, how to treat them efficiently. The discovery that adipose tissue is, in fact, an endocrine tissue able to secrete active molecules related to lipid homeostasis--the adipokines--has dramatically changed our understanding of the molecular events that take place in such diseases. This knowledge has been further improved by the discovery o...</description>
            <author>ENDOCR REV</author>
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            <pubDate>Sun, 14 May 2006 06:00:00 +0100</pubDate>
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