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.”

More on [ Endocrinology ]

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]

pubmed: 0804-4643

Outcomes of transsphenoidal surgery in prolactinomas: improvement of hormonal control in dopamine agonist resistant patients.
Primeau V, Raftopoulos C, Maiter D Outcomes of transsphenoidal surgery in prolactinomas: improvement of hormonal control in dopamine agonist resistant patients. Eur J Endocrinol. 2012 Feb 2; Authors: Primeau V, Raftopoulos C, Maiter D Abstract Context: Few studies have recently re-examined the efficacy of neurosurgery in prolactinoma patients operated for various indications.Objective: To analyze outcomes of patients with a prolactinoma treated by transsphenoidal surgery, to identify factors associated with remission and relapse and to evaluate if surgical debulking allows a better hormonal control in patients with preoperative resistance to dopamine agonists (DA).Patients and methods: This was a retrospective review of patients with a benign prolactinoma followed pre- and post-operatively in our Department and treated by transsphenoidal surgery (n=63; 45 women; mean age: 31 ± 14 years)Results: Post-operative remission was obtained in 63% of microprolactinomas, in 60% of non invasive macroprolactinomas and in none of the invasive macroprolactinomas. Better remission rate was independently predicted by lower diagnostic prolactin levels and the lack of abnormal postoperative residual tissue (p<0.05). A recurrence of hyperprolactinemia was observed in 34 % of the patients after a median follow-up period of 36 [7-164] months. In patients with preoperative DA resistance treated again after surgery, there was a significant reduction of prolactin levels postoperatively (26 [6-687] ng/ml) vs. preoperatively (70 [22-1514] ng/ml; p<0.01) under a lower DA dose, and about half of patients had prolactin normalization.Conclusions: Recurrence of hyperprolactinemia is observed in one third of prolactinoma patients after surgical remission and may occur as late as 13 years after surgery. Resistance to DA can be considered as a good surgical indication, as partial tumor resection allows a better hormonal control with a lower dose of dopamine agonists. PMID: 22301915 [PubMed - as supplied by publisher]
Evidence for association between paraoxonase 1 gene polymorphisms and polycystic ovarian syndrome (PCOS) in south-west Chinese women.
Wang Y, Liu H, Fan P, Bai H, Zhang J, Zhang F Evidence for association between paraoxonase 1 gene polymorphisms and polycystic ovarian syndrome (PCOS) in south-west Chinese women. Eur J Endocrinol. 2012 Feb 2; Authors: Wang Y, Liu H, Fan P, Bai H, Zhang J, Zhang F Abstract OBJCTIVE: The aim of this study was to investigate the relationship between 192Q/R and 55L/M polymorphisms of paraoxonase (PON) 1 gene and polycystic ovarian syndrome (PCOS) in Chinese women.DESIGN: A case-control study.METHODS: A total of one thousand one hundred thirteen subjects (610 patients with PCOS and 503 control women) from a population of Chinese Han nationality in Chengdu area were included in this study. PON1 genotypes were studied using PCR and restriction fragment length polymorphism analysis. Clinical and metabolic parameters were analyzed.RESULTS: The frequencies of PON1 192RR genotype and R allele were significantly higher in patients with PCOS than in control women (44.6 vs. 36.4%, 0.667 vs. 0.610, respectively). 192RR genotype remained a significant predictor for PCOS (odds ratio RR/QR+QQ: 1.656, 95%CI: 1.156-2.371) in prognostic models including age, body mass index (BMI), insulin resistance index, triglyceride, HDL and LDL as covariates. Compared with patients with QQ genotype, patients with RR or QR genotype had significantly higher waist circumference, fasting insulin and triglyceride levels, patients with RR genotype had significantly higher waist-to-hip ratio, and patients with QR genotype had significantly higher HOMA-IR. Such relationships were not detected in the control women. No significant differences were found in the frequencies of PON1 55L/M genotype and allele between PCOS and control groups.CONCLUSIONS: The 192Q/R, but not 55L/M, polymorphism in PON1 gene is associated with risk of PCOS in south-west Chinese women. PMID: 22301914 [PubMed - as supplied by publisher]
Mass Screening of Newborns for Congenital Hypothyroidism of Central Origin by Free Thyroxine Measurement of Blood Samples on Filter Paper.
Adachi M, Soneda A, Asakura Y, Muroya K, Yamagami Y, Hirahara F Mass Screening of Newborns for Congenital Hypothyroidism of Central Origin by Free Thyroxine Measurement of Blood Samples on Filter Paper. Eur J Endocrinol. 2012 Feb 2; Authors: Adachi M, Soneda A, Asakura Y, Muroya K, Yamagami Y, Hirahara F Abstract Objective: To evaluate the effectiveness of mass screening of newborns for congenital hypothyroidism of central origin (CH-C) by measurement of free T4 (FT4) and TSH.Design: Questionnaire-based survey of CH-C patients born between 1999 and 2008 in Kanagawa prefecture, Japan.Methods: TSH and FT4 levels in dried blood spots on filter paper were measured using ELISA kits, and CH-C was diagnosed at FT4 levels below a cutoff of 0.7 ng/dL (9.0 pmol/L). Survey results were collated with the database created by the screening organizer.Results: Twenty-four CH-C patients (18 males) were identified, 14 of whom had multiple pituitary hormone deficiencies (group M); 8, isolated CH-C (group I); and 2, undetermined pituitary involvement (group U). In groups M, I, and U, the number of patients with FT4 levels below the cutoff value at screening was 5 (36%), 7 (88%), and 1 (50%), respectively; other patients had been diagnosed clinically. Thus, 13 patients were true positives, while 9 were false negatives, yielding screening sensitivity of 59.1% and positive predictive value of 11.5%. The calculated sensitivity was 81.8% at a higher cutoff value of 0.9 ng/dL [11.6 pmol/L]. The overall incidence of CH-C was estimated at 1 in 30,833 live births, while that of congenital hypothyroidism of thyroidal origin (CH-T) is 1 in 3,472 live births in Kanagawa prefecture (CH-T/CH-C, 8.9).Conclusions: Newborn screening with combined FT4 and TSH measurements can identify a significant number of CH-C patients before manifestation of clinical symptoms, but a more appropriate FT4 cutoff value should be considered. PMID: 22301913 [PubMed - as supplied by publisher]
Elevated levels of the Steroidogenic Factor-1 are associated with over-expression of CYP19 in an Estrogen producing testicular Leydig cell tumour.
Straume AH, Løvås K, Miletic H, Gravdal K, Lønning PE, Knappskog S Elevated levels of the Steroidogenic Factor-1 are associated with over-expression of CYP19 in an Estrogen producing testicular Leydig cell tumour. Eur J Endocrinol. 2012 Feb 1; Authors: Straume AH, Løvås K, Miletic H, Gravdal K, Lønning PE, Knappskog S Abstract Background and objectivesTesticular leydig cell tumours (LCTs) are rare, steroid-secreting tumours. Elevated levels of aromatase (CYP19) mRNA have been described in LCTs previously, however little is known about the mechanism(s) causing CYP19 over-expression. We report a LCT in a 29 year old male with elevated plasma estradiol, caused by enhanced CYP19 transcription.Design and methodsWe measured intra-tumour expression of CYP19, and determined CYP19 promoter use by qPCR. Secondly, we explored CYP19 and promoter II (PII) for gene amplifications, and activating mutations in PII by sequencing. Third, we analysed intra-tumour expression of steroidogenic factor-1 (SF-1), liver receptor homologue-1 (LRH-1) and cyclooxygenase-2 (COX-2). Finally, we analysed SF-1 for promoter mutations and gene amplifications.ResultsSimilar to what has been recorded in normal Leydig cells; we found the bulk of tumour CYP19 transcripts to be PII-derived, excluding promoter-shift as a cause of enhanced transcription. Secondly, we excluded CYP19 and PII gene amplifications, and activating mutations in PII, as causes of elevated CYP19 mRNA. We found SF-1 mRNA to be up-regulated in the tumour, while LRH-1 and COX-2 were down-regulated. The finding of elevated SF-1 levels in the tumour was confirmed by immunohistochemistry. The elevated level of SF-1 was not due to promoter mutations or amplification of the SF-1 gene (NR5A1).ConclusionsOur results strongly suggests that the elevated levels of SF-1 have induced PII-regulated CYP19 transcription in this tumour. These findings are of relevance to the understanding of CYP19 up-regulation in general, which may occur in several tissues, including breast cancer. PMID: 22301800 [PubMed - as supplied by publisher]

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