RESEARCH BRIEFS

The following studies will be published in Endocrine Society journals. Before print, they are edited and posted online in each journal’s Early Release section. You can access the journals via www.endo-society.org.

Pancreatic PYY is a VDR target gene, further linking vitamin D signaling and energy metabolism regulation. Choi M, Ozeki J, Hashizume M, Kato S, Ishihara H, Makishima M. Vitamin D receptor activation induces peptide YY transcription in pancreatic islets.

Three subpopulations of ß cells are seen in mice expressing the green fluorescent protein under the control of the mouse insulin I gene promoter. Katsuta H, Aguayo-Mazzucato C, Katsuta R, et al. Subpopulations of GFP-marked mouse pancreatic ß-cells differs in size, granularity, and insulin secretion.

Apo AIV uses a CCK-dependent system and vagal nerves to relay its satiation signal to the rodent hindbrain. Lo CC, Langhans W, Georgievsky M, et al. Apolipoprotein AIV requires cholecystokinin and vagal nerves to suppress food intake.

Serum and ovarian chemerin levels are elevated in a 5α-dihydrotestosterone–induced rat PCOS model. Wang Q, Kim JY, Xue K, Liu J-y, Leader A, Tsang BK. Chemerin, a novel regulator of follicular steroidogenesis and its potential involvement in polycystic ovarian syndrome.

Disruption of the leptin gene in Sprague Dawley rats leads to increased body weight, hyperinsulinemia, glucose intolerance, immunosuppression, and increased bone mass. Vaira S, Yang C, McCoy A, et al. Creation and preliminary characterization of a leptin knockout rat.

Maternal height, adiposity, and serum vitamin D directly predict fetal femur size. Ioannou C, Javaid MK, Mahon P, et al. The effect of maternal vitamin D concentration on fetal bone.

In boys with Klinefelter syndrome, CNP production and clearance are increased, which may explain their overgrowth. Olney RC, Prickett TCR, Espiner EA, Ross JL. C-type natriuretic peptide (CNP) levels are altered in boys with Klinefelter syndrome.

Male-to-female transsexuals have a female-typical infundibular NKB system. Taziaux M, Swaab DF, Bakker J. Sex differences in the neurokinin B system in the human infundibular nucleus.

The BRAF V600E mutation is associated with lymph node metastases, stage, extrathyroidal extension, tumor size, male gender, multifocality, absence of capsule, classic PTC, and tall cell variant PTC. Li C, Lee KC, Schneider EB, Zeiger MA. BRAF V600E mutation and its association with clinic-pathologic features of papillary thyroid cancer: A meta-analysis.

As with seasonally obese animals, human BMI is linked with the time difference between the peak releases of prolactin and cortisol. Roelfsema F, Pijl H. Phase difference between serum prolactin and cortisol rhythms is related to body mass index in humans.

Computational screening platforms can be used to create AR antagonists that can be used in CRPC. Shen HC, Shanmugasundaram K, Simon NI, et al. In silico discovery of androgen receptor antagonists with activity in castration-resistant prostate cancer.

The plasma membrane expression level of gonadotropin-releasing hormone receptor regulates the interpretation of the GnRH signal by gonadotropes. Stewart MD, Deng JM, Stewart CA, et al. Mice harboring Gnrhr E90K, a mutation that causes protein misfolding and hypogonadotropic hypogonadism in humans, exhibit testis size reduction and ovulation failure.

In utero exposure to high fat alters the fetal thyroid axis and sets the stage for obesity in adulthood. Suter MA, Sangi-Haghpeykar H, Showalter L, et al. Maternal high fat diet modulates the fetal thyroid axis and thyroid gene expression in a nonhuman primate model.

Lowering glucose substrate and inhibiting pyruvate dehydrogenase may augment adjuvant therapies for ER-positive breast cancer. O’Mahony F, Razandi M, Pedram A, Harvey BJ, Levin ER. Estrogen modulates metabolic pathway adaptation to available glucose in breast cancer cells.

20-hydroxyeicosatetraenoic acid may be a potential new drug target for hypertension and hyperglycemia. Lai G, Wu J, Liu X, Zhao Y. 20-HETE induces hyperglycemia through the cAMP/PKA-PhK-GP pathway.

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