Endocrinology is a branch of medicine dealing with disorders of the endocrine system and its specific secretions called hormones. Hormones are molecules that act as signals from one type of cells to another. Most hormones reach their targets via the blood. Although every organ system secretes and responds to hormones (including the brain, lungs, heart, intestine, skin, and the kidney), the clinical specialty of endocrinology focuses primarily on the endocrine organs, meaning the organs whose primary function is hormone secretion. These organs include the pituitary, thyroid, adrenals, ovaries and testes, and pancreas.

An endocrinologist is a doctor who specializes in treating disorders of the endocrine system, such as diabetes, hyperthyroidism, and many others (see list of diseases below). A disease due to a disorder of the endocrine system is often called a "hormone imbalance," but is technically known as an endocrinopathy or endocrinosis.

Background

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All multicellular organisms need “Coordinating systems to regulate and integrate the function of differentiating cells.” Two mechanisms perform this function in higher animals: the nervous system and the endocrine system. The endocrine system acts through the release (generally into the blood) of chemical agents and is vital to the proper development and function of organisms. As Hadley (2000) notes, the integration of developmental events such as proliferation, growth, and differentiation (including histogenesis and organogenesis) and the coordination of metabolism, respiration, excretion, movement, reproduction, and sensory perception depend on “chemical cues, substances synthesised and secreted by the specialised cells within the animal.”

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Permanent Endocrinology Jobs

North Dartmouth :: Massachusetts :: New England Physician Recruitment Center
Tue, 09 Feb 2010 16:53:48 -0500
Endocrine-minutes to Boston and Providence. Salary and Compensation very, very competitive. Ideal Coastal Southern Massachusetts location. Outstanding opportunity for an additional BC/BE Endocrinologist
Williamstown :: Massachusetts :: New England Physician Recruitment Center
Tue, 09 Feb 2010 16:53:48 -0500
Subject: Endocrinology (predominately office based/no call) Great salary plus incentives plus productivity -College Town home of Williams College,Western Massachusetts- 4 day week, close to Albany,
Poughkeepsie :: New York :: New England Physician Recruitment Center
Tue, 09 Feb 2010 16:53:48 -0500
Endocrine Poughkeepsie, NY Southern NY, close to CT border and only 1 hour to NYC- join large multi specialty group with more than 55 providers. 15 primary care physicians. 3 office locations in the

pubmed: 0013-7227

Adenosine 5'-Monophosphate-Activated Protein Kinase-Mammalian Target of Rapamycin Cross Talk Regulates Brown Adipocyte Differentiation.
Vila-Bedmar R, Lorenzo M, Fernández-Veledo S Adenosine 5'-Monophosphate-Activated Protein Kinase-Mammalian Target of Rapamycin Cross Talk Regulates Brown Adipocyte Differentiation. Endocrinology. 2010 Feb 4; Authors: Vila-Bedmar R, Lorenzo M, Fernández-Veledo S Brown adipose tissue (BAT) is considered of metabolic significance in mammalian physiology, because it plays an important role in regulating energy balance. Alterations in this tissue have been associated with obesity and type 2 diabetes. The molecular mechanisms modulating brown adipocyte differentiation are not fully understood. Using a murine brown preadipocyte cell line, primary cultures, and 3T3-L1 cells, we analyzed the contribution of various intracellular signaling pathways to adipogenic and thermogenic programs. Sequential activation of p38MAPK and LKB1-AMPK-tuberous sclerosis complex 2 (TSC2) as well as significant attenuation of ERK1/2 and mammalian target of rapamycin (mTOR)-p70 S6 kinase 1 (p70S6K1) activation was observed through the brown differentiation process. This study demonstrates a critical role for AMPK in controlling the mTOR-p70S6K1 signaling cascade in brown but not in 3T3-L1 adipocytes. We observed that mTOR activity is essential in the first stages of differentiation. Nevertheless, subsequent inhibition of this cascade by AMPK activation is also necessary at later stages. An in vivo study showed that prolonged 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced AMPK activation increases uncoupling protein 1 expression and induces an accumulation of brown adipocytes in white adipose tissue (WAT), as revealed by immunohistology. Moreover, the induction of brown adipogenesis in areas of white fat partially correlates with the body weight reduction detected in response to treatment with AICAR. Taken together, our study reveals that differentiation of brown adipocytes employs different signaling pathways from white adipocytes, with AMPK-mTOR cross talk a central mediator of this process. Promotion of BAT development in WAT by pharmacological activation of AMPK may have potential in treating obesity by acting on energy dissipation. PMID: 20133456 [PubMed - as supplied by publisher]
Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence.
de Seranno S, d'Anglemont de Tassigny X, Estrella C, Loyens A, Kasparov S, Leroy D, Ojeda SR, Beauvillain JC, Prevot V Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence. Endocrinology. 2010 Feb 4; Authors: de Seranno S, d'Anglemont de Tassigny X, Estrella C, Loyens A, Kasparov S, Leroy D, Ojeda SR, Beauvillain JC, Prevot V In the ever-changing physiological context of the neuroendocrine brain, the mechanisms by which cellular events involving neurons, astroglia, and vascular cells are coordinated to bring forth the appropriate neuronal signaling is not yet known but is amenable to examination. In the median eminence of the hypothalamus, endothelial cells are key players in the plasticity of tanycytes (specialized astroglia) and neuroendocrine synapse efficacy. Here we report that estradiol acts on both purified endothelial cells and isolated tanycytes to trigger endothelial-to-glial communication that leads to a sudden and massive retraction of tanycyte processes. The blockade of endothelial nitric oxide synthase by in vitro adenoviral-mediated gene transfer of a dominant-negative form of endothelial nitric oxide synthase abrogates the estradiol-induced tanycyte plasticity mediated by endothelial cells. In parallel, increases in prostaglandin-E2 (PGE2) due to changes in cyclooxygenase (COX)-1 and COX-2 expression induced by the exposure of tanycytes to estradiol promote acute tanycyte plasticity. We also demonstrate by electron microscopy that the administration of PGE2 to median eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE2 synthesis in the median eminence of adult female rats with the COX inhibitor indomethacin impairs the ovarian cycle, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamo-hypophyseal portal system. Taken together, our findings show that estradiol controls the dialog between endothelial cells and astroglia to regulate neuroglial plasticity in the neuroendocrine brain. PMID: 20133455 [PubMed - as supplied by publisher]
The Levels of the Endocannabinoid Receptor CB2 and Its Ligand 2-Arachidonoylglycerol Are Elevated in Endometrial Carcinoma.
Guida M, Ligresti A, De Filippis D, D'Amico A, Petrosino S, Cipriano M, Bifulco G, Simonetti S, Orlando P, Insabato L, Nappi C, Di Spiezio Sardo A, Di Marzo V, Iuvone T The Levels of the Endocannabinoid Receptor CB2 and Its Ligand 2-Arachidonoylglycerol Are Elevated in Endometrial Carcinoma. Endocrinology. 2010 Feb 4; Authors: Guida M, Ligresti A, De Filippis D, D'Amico A, Petrosino S, Cipriano M, Bifulco G, Simonetti S, Orlando P, Insabato L, Nappi C, Di Spiezio Sardo A, Di Marzo V, Iuvone T The endocannabinoid system plays protective roles against the growth and the spreading of several types of carcinomas. Because estrogens regulate this system both in physiological states and cancer, in this paper we evaluated its involvement in endometrial carcinoma, a well-known estrogen-dependant tumor. To test whether the endocannabinoid system is expressed in endometrial cancer, tissue samples were collected both from 18 patients undergoing surgical treatment for endometrial adenocarcinoma and 16 healthy age-matched controls, and treated for Western blot and immunohistochemical analysis. Moreover, tissues were dounce homogenized and submitted to endocannabinoid measurement by liquid chromatography-mass spectrometry. To evaluate the physiological role of the endocannabinoid system, a human endometrial cancer cell-line (AN3CA) was used and transiently transfected with a plasmid containing the cDNA for the endocannabinoid receptor CB2. Cells were incubated for 48 h with an agonist (JWH133) (10 muM) or antagonist (SR144528) (1 muM) of CB2 24 h after transfection, and cell proliferation was measured by the 3-[4,5-dimethyltiazol-2yl]-2,5 diphenyltetrazolium bromide formazan assay. In human endometrial carcinoma biopsies the expression of CB2 receptor and the levels of its ligand, 2-arachidonoylglycerol increased, whereas monoacylglyerol lipase, an enzyme responsible for 2-arachidonoylglycerol degradation, was down-regulated. Immunohystochemical analysis revealed that CB2 was overexpressed only in malignant endometrial cells. CB2-overexpressing AN3CA cells showed a significant reduction in cell vitality compared with parental AN3CA cells: incubation with the selective CB2 antagonist SR144128 restored the viability of CB2-overexpressing cells to that of untransfected cells. In conclusion, the endocannabinoid system seems to play an important role in human endometrial carcinoma, and modulation of CB2 activity/expression may account for a tumor-suppressive effect. PMID: 20133454 [PubMed - as supplied by publisher]
Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma.
Lu C, Zhao L, Ying H, Willingham MC, Cheng SY Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma. Endocrinology. 2010 Feb 4; Authors: Lu C, Zhao L, Ying H, Willingham MC, Cheng SY TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRbeta(PV/PV) mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-beta receptor (TRbeta), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRbeta(PV/PV) mice were crossed with TSH receptor gene knockout (TSHR(-/-)) mice. Wild-type siblings of TRbeta(PV/PV) mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRbeta(PV/PV)TSHR(-/-) showed impaired growth with no occurrence of FTC. Both WT-PTU and TRbeta(PV/PV) mice displayed enlarged thyroids, but only TRbeta(PV/PV) mice developed metastatic FTC. Molecular analyses indicate that PV acted, via multiple mechanisms, to activate the integrins-Src-focal adhesion kinase-p38 MAPK pathway and affect cytoskeletal restructuring to increase tumor cell migration and invasion. Thus, growth stimulated by TSH is a prerequisite but not sufficient for metastatic cancer to occur. Additional genetic alterations (such as PV), destined to alter focal adhesion and migration capacities, are required to empower hyperplastic follicular cells to invade and metastasize. These in vivo findings provide new insights in understanding carcinogenesis of the human thyroid. PMID: 20133453 [PubMed - as supplied by publisher]
Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet.
Drake AJ, Raubenheimer PJ, Kerrigan D, McInnes KJ, Seckl JR, Walker BR Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet. Endocrinology. 2010 Feb 4; Authors: Drake AJ, Raubenheimer PJ, Kerrigan D, McInnes KJ, Seckl JR, Walker BR The association between low birth weight and cardiovascular disease is amplified by the development of obesity. We explored the effects of postnatal high-fat (HF) feeding in dexamethasone (Dex)-programmed rats, in which prenatal glucocorticoid overexposure is associated with reduced birth weight and adult glucose intolerance. Male Wistar rats exposed to Dex or vehicle (Veh) during the last week of gestation were weaned onto HF or control diets for 6 months. Dex-exposed animals were of lower birth weight and showed catch-up growth by 7 wk. There were no differences in obesity or hyperinsulinaemia between Dex-HF and Veh-HF animals. However, Dex-HF animals had increased hepatic triglyceride content compared with Veh-HF animals. mRNA transcript profiles in adipose tissue revealed depot-specific changes in the expression of genes involved in fatty acid esterification and triglyceride synthesis and storage with prenatal Dex exposure. Thus, antenatal glucocorticoid overexposure in rats does not confer increased sensitivity to HF diet-induced obesity, but increases susceptibility to fatty liver. This may be due to depot-specific-programmed alterations in fat metabolism in adipose tissue. PMID: 20133452 [PubMed - as supplied by publisher]
15-Deoxy-{Delta}12-14-Prostaglandin-J2 Induces Hypertrophy and Loss of Contractility in Human Testicular Peritubular Cells: Implications for Human Male Fertility.
Schell C, Albrecht M, Spillner S, Mayer C, Kunz L, Köhn FM, Schwarzer U, Mayerhofer A 15-Deoxy-{Delta}12-14-Prostaglandin-J2 Induces Hypertrophy and Loss of Contractility in Human Testicular Peritubular Cells: Implications for Human Male Fertility. Endocrinology. 2010 Feb 4; Authors: Schell C, Albrecht M, Spillner S, Mayer C, Kunz L, Köhn FM, Schwarzer U, Mayerhofer A The wall of the seminiferous tubules contains contractile smooth-muscle-like peritubular cells, thought to be important for sperm transport. Impaired spermatogenesis in men typically involves remodeling of this wall, and we now found that smooth muscle cell (SMC) markers, namely myosin heavy chain (MYH11) and smooth muscle actin (SMA) are often lost or diminished in peritubular cells of testes of men with impaired spermatogenesis. This suggests reduced contractility of the peritubular wall, which may contribute to sub- or infertility. In these cases, testicular expression of cyclooxygenase-2 (COX-2) implies formation of prostaglandins (PGs). When screening different PGs for their ability to target human testicular peritubular cells (HTPCs), only a PG metabolite, 15-deoxy-Delta(12-14)-prostaglandin-J2 (15dPGJ2), was effective. In primary cultures of HTPCs, 15dPGJ2 increased cell size in a reversible manner. Importantly, 15dPGJ2 treatment resulted in a loss of typical differentiation markers for SMCs, namely MYH11, calponin, and SMA, whereas fibroblast markers were unchanged. Collagen gel contraction assays revealed that this loss correlates with a reduced ability to contract. Experiments with an antagonist (bisphenol A diglycidyl ether) and agonist (troglitazone) for a cognate 15dPGJ2 receptor (i.e. peroxisome proliferator-activated receptor-gamma) indicated that peroxisome proliferator-activated receptor-gamma is not directly involved. Rather, the mode of action of 15dPGJ2 involves reactive oxygen species. The antioxidant N-acetylcysteine not only blocked ROS formation but also prevented the increase in cell size and the loss of contractility in HTPCs challenged with 15dPGJ2. We conclude that 15dPGJ2, via reactive oxygen species, influences SMC phenotype and contractility of human peritubular cells and possibly is involved in the development of human male sub-/infertility. PMID: 20133451 [PubMed - as supplied by publisher]

pubmed: 0804-4643

Cholecalciferol loading dose guideline for vitamin D deficient adults.
van Groningen L, Opdenoordt S, van Sorge A, Telting D, Giesen A, de Boer H Cholecalciferol loading dose guideline for vitamin D deficient adults. Eur J Endocrinol. 2010 Feb 5; Authors: van Groningen L, Opdenoordt S, van Sorge A, Telting D, Giesen A, de Boer H Introduction: Severe vitamin D deficiency is very common. Evidence-based guidelines for rapid correction with high dose oral cholecalciferol are not available yet. Objective: To develop a practical cholecalciferol loading dose regimen. Materials and methods: 208 vitamin D deficient subjects (serum 25-OH vitamin D3 level < 50 nmol/L), age 18 - 88 years, were treated with solubilised cholecalciferol 50.000 IU/ml. They either received 25.000 IU every fortnight for 8 weeks (total dose 100.000 IU), 25.000 IU every week for 6 weeks (total dose 150.000 IU), or 25.000 IU every week for 8 weeks (total dose 200.000 IU). Blood samples were taken at baseline and 10 days after the final dose of cholecalciferol. Results: Most patients were severely vitamin D deficient: 76% had a serum 25-OHD3 level < 30 nmol/L at baseline. Cholecalciferol in a cumulative dose of 100.000 IU, 150.000 IU and 200.000 IU increased mean serum 25-OHD3 by 29 nmol/L (95% CI: 23 - 35 nmol/L), 43 nmol/L (95% CI: 36 - 50 nmol/L), and 69 nmol/L (95% CI: 64 - 75 nmol/L), respectively. The change in 25-OHD3 (25-OHD3) was related to the dose per kilogram body weight (R2 = 0.38, P < 0.0001), and is described by the equation 25-OHD3 = 0.025 x (dose per kg body weight). Conclusion: The cholecalciferol loading dose required to reach the serum 25-OHD3 target level of 75 nmol/L can be calculated as follows: Dose (IU) = 40 x (75 - serum 25-OHD3) x Body Weight. PMID: 20139241 [PubMed - as supplied by publisher]

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