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pubmed: 0013-7227
Glucagon in Stress and Energy Homeostasis.
Jones BJ, Tan T, Bloom SR Glucagon in Stress and Energy Homeostasis. Endocrinology. 2012 Jan 31; Authors: Jones BJ, Tan T, Bloom SR Abstract Glucagon is traditionally thought of as an antihypoglycemic hormone, for example in response to starvation. However, it actually increases energy expenditure and has other actions not in line with protection from hypoglycemia. Furthermore, it is often found to be elevated when glucose is also raised, for example in circumstances of psychological and metabolic stress. These findings seem more in keeping with glucagon having some role as a hormone enhancing the response to stress. PMID: 22294753 [PubMed - as supplied by publisher]
Dynamic Regulation of Wnt7a Expression in the Primate Endometrium: Implications for Postmenstrual Regeneration and Secretory Transformation.
Fan X, Krieg S, Hwang JY, Dhal S, Kuo CJ, Lasley BL, Brenner RM, Nayak NR Dynamic Regulation of Wnt7a Expression in the Primate Endometrium: Implications for Postmenstrual Regeneration and Secretory Transformation. Endocrinology. 2012 Jan 31; Authors: Fan X, Krieg S, Hwang JY, Dhal S, Kuo CJ, Lasley BL, Brenner RM, Nayak NR Abstract Despite the vital physiological role of endometrial regeneration during the menstrual cycle and the various pathological implications of abnormal growth of endometrial epithelial cells, the local factors and regulatory mechanisms involved in endometrial regeneration and growth have not been well characterized. Here, we examine the pattern, hormone dependence, and potential functions of Wnt7a (wingless-type MMTV integration site family member 7a), , which is known to play a critical role in the formation of the mouse endometrial epithelium during embryonic development, in both human and artificially cycling rhesus macaque endometrium, and using a potent Wnt-antagonist in a mouse model of endometrial regeneration. Wnt7a transcript levels were examined using quantitative real-time PCR and in situ hybridization, and immunohistochemistry was performed to detect Ki-67 and 3,5-bromodeoxyuridine. Stringent, fully conditional Wnt inhibition was achieved by adenoviral expression of Dickkopf-1 during artificial endometrial regeneration in mice. In macaques, Wnt7a expression was confined to the newly formed luminal epithelium (LE) and upper glands during the postmenstrual repair phase. The signal increased in the LE during the proliferative phase but decreased in the upper glands and was undetectable in the glands by the late proliferative phase. Interestingly, Wnt7a was completely suppressed in the LE and remained undetectable in other cell types after 7 d of progesterone treatment. The pattern of Wnt7a expression in the human endometrium was similar to that in macaques. Blockade of Wnt signaling during endometrial regeneration in mice resulted in a dramatic delay in reepithelialization and degeneration of glands and LE. These results strongly suggest, for the first time, a role for Wnt7a in postmenstrual regeneration and proliferation of endometrial glands and LE in primates, and its dramatic suppression by progesterone is likely essential for secretory transformation of the epithelium. PMID: 22294752 [PubMed - as supplied by publisher]
Live Imaging Reveals the Link Between Decreased Glucose Uptake in Ovarian Cumulus Cells and Impaired Oocyte Quality in Female Diabetic Mice.
Wang Q, Chi MM, Moley KH Live Imaging Reveals the Link Between Decreased Glucose Uptake in Ovarian Cumulus Cells and Impaired Oocyte Quality in Female Diabetic Mice. Endocrinology. 2012 Jan 31; Authors: Wang Q, Chi MM, Moley KH Abstract Maternal diabetes has been demonstrated to adversely affect preimplantation embryo development and pregnancy outcomes. Emerging data suggest that these effects are associated with compromised oocyte quality. However, direct evidence of a pathway by which maternal diabetes exerts its effects on the oocyte is still lacking. Cumulus cells are metabolically coupled to oocytes, and bidirectional communication between them is essential for the development and functions of both compartments. The primary focus of this work was to evaluate the connection between glucose uptake in cumulus cells and oocyte quality in diabetic mice. This experiment has been difficult, because cumulus cells need to be separated from oocytes and labeled with isotope in the process of measuring glucose uptake. Here, we report a method for live imaging glucose transport in single cumulus-oocyte complexes using a fluorescent glucose analog (6-(N-(7-nitrobenz-2-oxa-1,3-diazol- 4-yl)amino)-6-deoxyglucose). By tracking the ATP content and spindle/chromosome status in individual oocytes surrounded by cumulus cells with differing glucose uptake activity, we reveal that compromised oocyte quality in diabetic mice is linked to decreased glucose uptake in cumulus cells. PMID: 22294751 [PubMed - as supplied by publisher]
Long-Term Fgf23 Deficiency Does Not Influence Aging, Glucose Homeostasis, or Fat Metabolism in Mice with a Nonfunctioning Vitamin D Receptor.
Streicher C, Zeitz U, Andrukhova O, Rupprecht A, Pohl E, Larsson TE, Windisch W, Lanske B, Erben RG Long-Term Fgf23 Deficiency Does Not Influence Aging, Glucose Homeostasis, or Fat Metabolism in Mice with a Nonfunctioning Vitamin D Receptor. Endocrinology. 2012 Jan 31; Authors: Streicher C, Zeitz U, Andrukhova O, Rupprecht A, Pohl E, Larsson TE, Windisch W, Lanske B, Erben RG Abstract It is still controversial whether the bone-derived hormone fibroblast growth factor-23 (FGF23) has additional physiological functions apart from its well-known suppressive actions on renal phosphate reabsorption and vitamin D hormone synthesis. Here we analyzed premature aging, mineral homeostasis, carbohydrate metabolism, and fat metabolism in 9-month-old male wild-type (WT) mice, vitamin D receptor mutant mice (VDR(Δ)(/)(Δ)) with a nonfunctioning vitamin D receptor, and Fgf23(-/-)/VDR(Δ)(/)(Δ) compound mutant mice on both a standard rodent chow and a rescue diet enriched with calcium, phosphorus, and lactose. Organ atrophy, lung emphysema, and ectopic tissue or vascular calcifications were absent in compound mutants. In addition, body weight, glucose tolerance, insulin tolerance, insulin secretory capacity, pancreatic beta cell volume, and retroperitoneal and epididymal fat mass as well as serum cholesterol and triglycerides were indistinguishable between vitamin D receptor and compound mutants. In contrast to VDR(Δ)(/)(Δ) and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice, which stayed lean, WT mice showed obesity-induced insulin resistance. To rule out alopecia and concomitantly elevated energy expenditure present in 9-month-old VDR(Δ)(/)(Δ) and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice as a confounding factor for the lacking effect of Fgf23 deficiency on fat mass, we analyzed whole-body composition in WT, Fgf23(-/-), VDR(Δ)(/)(Δ), and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice at the age of 4 wk, when the coat in VDR(Δ)(/)(Δ) mice is still normal. Whole-body fat mass was reduced in Fgf23(-/-) mice but almost identical in WT, VDR(Δ)(/)(Δ), and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice. In conclusion, our data indicate that Fgf23 has no molecular vitamin D-independent role in aging, insulin signaling, or fat metabolism in mice. PMID: 22294750 [PubMed - as supplied by publisher]
FOXL2 Is Involved in the Synergy between Activin and Progestins on the Follicle-Stimulating Hormone β-Subunit Promoter.
Ghochani Y, Saini JK, Mellon PL, Thackray VG FOXL2 Is Involved in the Synergy between Activin and Progestins on the Follicle-Stimulating Hormone β-Subunit Promoter. Endocrinology. 2012 Jan 31; Authors: Ghochani Y, Saini JK, Mellon PL, Thackray VG Abstract Differential regulation of gonadotropin hormone production in the pituitary is critical for fertility. Activin and progesterone signaling in gonadotrope cells is important for Fshb gene expression. Previously, we reported that synergy between activin and progestins required the binding of SMAD proteins and the progesterone receptor (PR) to the murine Fshb promoter. In this study, we demonstrate that the FOXL2 transcription factor is also necessary for the full synergistic response between activin and progestins. We show that this synergy occurs in a species-specific manner and that multiple elements in the Fshb promoter that bind forkhead box L2 (FOXL2), SMA/mothers against decapentaplegic homologs (SMAD), and PR are required. Furthermore, we demonstrate that FOXL2 can physically interact with PR and SMAD3. Thus, it is likely that protein-protein interactions among FOXL2, SMAD, and PR recruited to the Fshb promoter play a key role in facilitating Fshb transcription before the secondary FSH surge in rodents. PMID: 22294749 [PubMed - as supplied by publisher]
The Ubiquitin Ligase Siah2 Regulates PPARγ Activity in Adipocytes.
Kilroy G, Kirk-Ballard H, Carter LE, Floyd ZE The Ubiquitin Ligase Siah2 Regulates PPARγ Activity in Adipocytes. Endocrinology. 2012 Jan 31; Authors: Kilroy G, Kirk-Ballard H, Carter LE, Floyd ZE Abstract Moderate reductions in peroxisome proliferator-activated receptor (PPAR)γ levels control insulin sensitivity as effectively as activation of PPARγ in adipocytes by the thiazolidinediones. That observation suggests that PPARγ activity can be regulated by modulating the amount of PPARγ protein in adipocytes. Activation of PPARγ in adipocytes is linked to changes in PPARγ protein levels via increased degradation of PPARγ proteins by the ubiquitin proteasome system. Identification of the ubiquitin ligase or ligases that recognize ligand bound PPARγ is an essential step in determining the physiological significance of the relationship between activation and ubiquitin-dependent degradation of PPARγ. Using an RNA interference-based screen, we identified five RING (really interesting new gene)-type ubiquitin ligases that alter PPARγ protein levels in adipocytes. Here, we demonstrate that Drosophila seven-in-absentia homolog 2 (Siah2), a mammalian homolog of Drosophila seven-in-absentia, regulates PPARγ ubiquitylation and ligand-dependent activation of PPARγ in adipocytes. We also demonstrate that Siah2 expression is up-regulated during adipogenesis and that PPARγ interacts with Siah2 during adipogenesis. In addition, Siah2 is required for adipogenesis. These data suggest that modulation of PPARγ protein levels by the ubiquitin ligase Siah2 is essential in determining the physiological effects of PPARγ activation in adipocytes. PMID: 22294748 [PubMed - as supplied by publisher]
Evidence for Differential Regulation of GnRH Signaling via Heterodimerization among GnRH Receptor Paralogs in the Protochordate, Ciona intestinalis.
Sakai T, Aoyama M, Kawada T, Kusakabe T, Tsuda M, Satake H Evidence for Differential Regulation of GnRH Signaling via Heterodimerization among GnRH Receptor Paralogs in the Protochordate, Ciona intestinalis. Endocrinology. 2012 Jan 31; Authors: Sakai T, Aoyama M, Kawada T, Kusakabe T, Tsuda M, Satake H Abstract The endocrine and neuroendocrine systems for reproductive functions have diversified as a result of the generation of species-specific paralogs of peptide hormones and their receptors including GnRH and their receptors (GnRHR), which belong to the class A G protein-coupled receptor family. A protochordate, Ciona intestinalis, has been found to possess seven GnRH (tGnRH-3 to -8 and Ci-GnRH-X) and four GnRHR (Ci-GnRHR1 to -4). Moreover, Ci-GnRHR4 (R4) does not bind to any Ciona GnRH and activate any signaling pathways. Here we show novel functional diversification of GnRH signaling pathways via G protein-coupled receptor heterodimerization among Ciona GnRHR. R4 was shown
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Glucagon in Stress and Energy Homeostasis.
Jones BJ, Tan T, Bloom SR Glucagon in Stress and Energy Homeostasis. Endocrinology. 2012 Jan 31; Authors: Jones BJ, Tan T, Bloom SR Abstract Glucagon is traditionally thought of as an antihypoglycemic hormone, for example in response to starvation. However, it actually increases energy expenditure and has other actions not in line with protection from hypoglycemia. Furthermore, it is often found to be elevated when glucose is also raised, for example in circumstances of psychological and metabolic stress. These findings seem more in keeping with glucagon having some role as a hormone enhancing the response to stress. PMID: 22294753 [PubMed - as supplied by publisher]
Dynamic Regulation of Wnt7a Expression in the Primate Endometrium: Implications for Postmenstrual Regeneration and Secretory Transformation.
Fan X, Krieg S, Hwang JY, Dhal S, Kuo CJ, Lasley BL, Brenner RM, Nayak NR Dynamic Regulation of Wnt7a Expression in the Primate Endometrium: Implications for Postmenstrual Regeneration and Secretory Transformation. Endocrinology. 2012 Jan 31; Authors: Fan X, Krieg S, Hwang JY, Dhal S, Kuo CJ, Lasley BL, Brenner RM, Nayak NR Abstract Despite the vital physiological role of endometrial regeneration during the menstrual cycle and the various pathological implications of abnormal growth of endometrial epithelial cells, the local factors and regulatory mechanisms involved in endometrial regeneration and growth have not been well characterized. Here, we examine the pattern, hormone dependence, and potential functions of Wnt7a (wingless-type MMTV integration site family member 7a), , which is known to play a critical role in the formation of the mouse endometrial epithelium during embryonic development, in both human and artificially cycling rhesus macaque endometrium, and using a potent Wnt-antagonist in a mouse model of endometrial regeneration. Wnt7a transcript levels were examined using quantitative real-time PCR and in situ hybridization, and immunohistochemistry was performed to detect Ki-67 and 3,5-bromodeoxyuridine. Stringent, fully conditional Wnt inhibition was achieved by adenoviral expression of Dickkopf-1 during artificial endometrial regeneration in mice. In macaques, Wnt7a expression was confined to the newly formed luminal epithelium (LE) and upper glands during the postmenstrual repair phase. The signal increased in the LE during the proliferative phase but decreased in the upper glands and was undetectable in the glands by the late proliferative phase. Interestingly, Wnt7a was completely suppressed in the LE and remained undetectable in other cell types after 7 d of progesterone treatment. The pattern of Wnt7a expression in the human endometrium was similar to that in macaques. Blockade of Wnt signaling during endometrial regeneration in mice resulted in a dramatic delay in reepithelialization and degeneration of glands and LE. These results strongly suggest, for the first time, a role for Wnt7a in postmenstrual regeneration and proliferation of endometrial glands and LE in primates, and its dramatic suppression by progesterone is likely essential for secretory transformation of the epithelium. PMID: 22294752 [PubMed - as supplied by publisher]
Live Imaging Reveals the Link Between Decreased Glucose Uptake in Ovarian Cumulus Cells and Impaired Oocyte Quality in Female Diabetic Mice.
Wang Q, Chi MM, Moley KH Live Imaging Reveals the Link Between Decreased Glucose Uptake in Ovarian Cumulus Cells and Impaired Oocyte Quality in Female Diabetic Mice. Endocrinology. 2012 Jan 31; Authors: Wang Q, Chi MM, Moley KH Abstract Maternal diabetes has been demonstrated to adversely affect preimplantation embryo development and pregnancy outcomes. Emerging data suggest that these effects are associated with compromised oocyte quality. However, direct evidence of a pathway by which maternal diabetes exerts its effects on the oocyte is still lacking. Cumulus cells are metabolically coupled to oocytes, and bidirectional communication between them is essential for the development and functions of both compartments. The primary focus of this work was to evaluate the connection between glucose uptake in cumulus cells and oocyte quality in diabetic mice. This experiment has been difficult, because cumulus cells need to be separated from oocytes and labeled with isotope in the process of measuring glucose uptake. Here, we report a method for live imaging glucose transport in single cumulus-oocyte complexes using a fluorescent glucose analog (6-(N-(7-nitrobenz-2-oxa-1,3-diazol- 4-yl)amino)-6-deoxyglucose). By tracking the ATP content and spindle/chromosome status in individual oocytes surrounded by cumulus cells with differing glucose uptake activity, we reveal that compromised oocyte quality in diabetic mice is linked to decreased glucose uptake in cumulus cells. PMID: 22294751 [PubMed - as supplied by publisher]
Long-Term Fgf23 Deficiency Does Not Influence Aging, Glucose Homeostasis, or Fat Metabolism in Mice with a Nonfunctioning Vitamin D Receptor.
Streicher C, Zeitz U, Andrukhova O, Rupprecht A, Pohl E, Larsson TE, Windisch W, Lanske B, Erben RG Long-Term Fgf23 Deficiency Does Not Influence Aging, Glucose Homeostasis, or Fat Metabolism in Mice with a Nonfunctioning Vitamin D Receptor. Endocrinology. 2012 Jan 31; Authors: Streicher C, Zeitz U, Andrukhova O, Rupprecht A, Pohl E, Larsson TE, Windisch W, Lanske B, Erben RG Abstract It is still controversial whether the bone-derived hormone fibroblast growth factor-23 (FGF23) has additional physiological functions apart from its well-known suppressive actions on renal phosphate reabsorption and vitamin D hormone synthesis. Here we analyzed premature aging, mineral homeostasis, carbohydrate metabolism, and fat metabolism in 9-month-old male wild-type (WT) mice, vitamin D receptor mutant mice (VDR(Δ)(/)(Δ)) with a nonfunctioning vitamin D receptor, and Fgf23(-/-)/VDR(Δ)(/)(Δ) compound mutant mice on both a standard rodent chow and a rescue diet enriched with calcium, phosphorus, and lactose. Organ atrophy, lung emphysema, and ectopic tissue or vascular calcifications were absent in compound mutants. In addition, body weight, glucose tolerance, insulin tolerance, insulin secretory capacity, pancreatic beta cell volume, and retroperitoneal and epididymal fat mass as well as serum cholesterol and triglycerides were indistinguishable between vitamin D receptor and compound mutants. In contrast to VDR(Δ)(/)(Δ) and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice, which stayed lean, WT mice showed obesity-induced insulin resistance. To rule out alopecia and concomitantly elevated energy expenditure present in 9-month-old VDR(Δ)(/)(Δ) and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice as a confounding factor for the lacking effect of Fgf23 deficiency on fat mass, we analyzed whole-body composition in WT, Fgf23(-/-), VDR(Δ)(/)(Δ), and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice at the age of 4 wk, when the coat in VDR(Δ)(/)(Δ) mice is still normal. Whole-body fat mass was reduced in Fgf23(-/-) mice but almost identical in WT, VDR(Δ)(/)(Δ), and Fgf23(-/-)/VDR(Δ)(/)(Δ) mice. In conclusion, our data indicate that Fgf23 has no molecular vitamin D-independent role in aging, insulin signaling, or fat metabolism in mice. PMID: 22294750 [PubMed - as supplied by publisher]
FOXL2 Is Involved in the Synergy between Activin and Progestins on the Follicle-Stimulating Hormone β-Subunit Promoter.
Ghochani Y, Saini JK, Mellon PL, Thackray VG FOXL2 Is Involved in the Synergy between Activin and Progestins on the Follicle-Stimulating Hormone β-Subunit Promoter. Endocrinology. 2012 Jan 31; Authors: Ghochani Y, Saini JK, Mellon PL, Thackray VG Abstract Differential regulation of gonadotropin hormone production in the pituitary is critical for fertility. Activin and progesterone signaling in gonadotrope cells is important for Fshb gene expression. Previously, we reported that synergy between activin and progestins required the binding of SMAD proteins and the progesterone receptor (PR) to the murine Fshb promoter. In this study, we demonstrate that the FOXL2 transcription factor is also necessary for the full synergistic response between activin and progestins. We show that this synergy occurs in a species-specific manner and that multiple elements in the Fshb promoter that bind forkhead box L2 (FOXL2), SMA/mothers against decapentaplegic homologs (SMAD), and PR are required. Furthermore, we demonstrate that FOXL2 can physically interact with PR and SMAD3. Thus, it is likely that protein-protein interactions among FOXL2, SMAD, and PR recruited to the Fshb promoter play a key role in facilitating Fshb transcription before the secondary FSH surge in rodents. PMID: 22294749 [PubMed - as supplied by publisher]
The Ubiquitin Ligase Siah2 Regulates PPARγ Activity in Adipocytes.
Kilroy G, Kirk-Ballard H, Carter LE, Floyd ZE The Ubiquitin Ligase Siah2 Regulates PPARγ Activity in Adipocytes. Endocrinology. 2012 Jan 31; Authors: Kilroy G, Kirk-Ballard H, Carter LE, Floyd ZE Abstract Moderate reductions in peroxisome proliferator-activated receptor (PPAR)γ levels control insulin sensitivity as effectively as activation of PPARγ in adipocytes by the thiazolidinediones. That observation suggests that PPARγ activity can be regulated by modulating the amount of PPARγ protein in adipocytes. Activation of PPARγ in adipocytes is linked to changes in PPARγ protein levels via increased degradation of PPARγ proteins by the ubiquitin proteasome system. Identification of the ubiquitin ligase or ligases that recognize ligand bound PPARγ is an essential step in determining the physiological significance of the relationship between activation and ubiquitin-dependent degradation of PPARγ. Using an RNA interference-based screen, we identified five RING (really interesting new gene)-type ubiquitin ligases that alter PPARγ protein levels in adipocytes. Here, we demonstrate that Drosophila seven-in-absentia homolog 2 (Siah2), a mammalian homolog of Drosophila seven-in-absentia, regulates PPARγ ubiquitylation and ligand-dependent activation of PPARγ in adipocytes. We also demonstrate that Siah2 expression is up-regulated during adipogenesis and that PPARγ interacts with Siah2 during adipogenesis. In addition, Siah2 is required for adipogenesis. These data suggest that modulation of PPARγ protein levels by the ubiquitin ligase Siah2 is essential in determining the physiological effects of PPARγ activation in adipocytes. PMID: 22294748 [PubMed - as supplied by publisher]
Evidence for Differential Regulation of GnRH Signaling via Heterodimerization among GnRH Receptor Paralogs in the Protochordate, Ciona intestinalis.
Sakai T, Aoyama M, Kawada T, Kusakabe T, Tsuda M, Satake H Evidence for Differential Regulation of GnRH Signaling via Heterodimerization among GnRH Receptor Paralogs in the Protochordate, Ciona intestinalis. Endocrinology. 2012 Jan 31; Authors: Sakai T, Aoyama M, Kawada T, Kusakabe T, Tsuda M, Satake H Abstract The endocrine and neuroendocrine systems for reproductive functions have diversified as a result of the generation of species-specific paralogs of peptide hormones and their receptors including GnRH and their receptors (GnRHR), which belong to the class A G protein-coupled receptor family. A protochordate, Ciona intestinalis, has been found to possess seven GnRH (tGnRH-3 to -8 and Ci-GnRH-X) and four GnRHR (Ci-GnRHR1 to -4). Moreover, Ci-GnRHR4 (R4) does not bind to any Ciona GnRH and activate any signaling pathways. Here we show novel functional diversification of GnRH signaling pathways via G protein-coupled receptor heterodimerization among Ciona GnRHR. R4 was shown
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Diabetes Physicians: Find a Portland doctor in the OHSU Medical Group. Find a Doctor by name, health condition or specialty.Endocrine Surgeon: EndocrineSurgeon.co.uk - the Endocrine Surgery web site, focusing on problems with the thyroid, parathyroid and adrenal glands
EndocrineWeb: Large award winning site written by doctors and patients FOR PATIENTS. Over 200 pages and illustrations for thyroid, parathyroid and adrenal. Find a local doctor, support group or join the chat rooms. Updated daily, includes the newest treatments; new pages weekly.
Endocrinology Section - University of Chicago: Information on endocrine disorders and diseases from the highly esteemed Endocrinology Section at the University of Chicago Medical Center.
Endocrinology.com: A site dedicated to the study of Endocrinology
EndoLinx: Features peer-reviewed endocrinology articles, news, newsletters, CME, conferences, and medical dictionaries. EndoLinx and MDLinx aggregate for physicians, health care professionals, residents, med students the most current medical news, journals, and research.
Family Practice Notebook - Endocrinology: Contains Adrenal Disease, Diabetes Mellitus, Examination, Growth, Hypoglycemia, Metabolism, Obesity, Parathyroid Disease, Pituitary Disease, Sex, Symptom Evaluation and Thyroid Disease. Related chapters from other specialties include Dermatology, Ophthalmology, Geriatric, Hematology and Oncology...
Medscape: Diabetes and Endocrinology: Medscape Diabetes and Endocrinology is a free resource for Physicians, featuring Free Diabetes and Endocrinology CME (Continuing Medical Education), Diabetes and Endocrinology medical journal articles, MEDLINE, Diabetes and Endocrinology medical news, major Diabetes and Endocrinology conference c...
National Diabetes Education Initiative: National Diabetes Education Initiative - Slides, Online CME, Events and Literature Alerts.
Online Endocrinology Journals: Free full-text access to Endocrine-Related Cancer, free access to reviews and commentaries and searchable advance abstracts from the Journal of Endocrinology and the Journal of Molecular Endocrinology.
ThyroidToday: Provides information on the causes, diagnosis, latest findings, and treatment of various forms of the disease.
UCLA Pituitary Tumor and Neuroendocrine Program: The UCLA Pituitary Tumor and Neuroendocrine Program directed by Dr. Daniel F. Kelly provides comprehensive evaluation and treatment of patients with pituitary tumors and related neuroendocrine disorders.
