Anti-Fshb polyclonal antibody

Context: A polymorphism in the FSHB promoter (-211G -> T, rs10835638) was found to be associated with decreased FSH, elevated LH, reduced testosterone, and oligozoospermia in males. Although FSH is pivotal for ovarian function, no data on consequences of FSHB -211G -> T are available in females. Objective: We studied the effects of FSHB -211G -> T on the hypothalamic- pituitary-ovarian axis in women. Design and Setting: In a university-based in vitro fertilization unit, women undergoing standardized diagnostics were genotyped and compared with a fertile control group. Patients: The study group consisted of 365 thoroughly characterized women with normal menstrual cycle intervals and proven ovulation, with predominantly male-factor infertility. The independently recruited control group included 438 women with proven fertility and no history of abortions. Main Outcome Measures: Distribution of alleles and genotypes were compared between the study group and controls. In the study group, associations of endocrine parameters with FSHB -211G -> T were assessed. Results: Allele and genotype frequencies were not significantly different between the study population and controls (T-allele: 14.4 vs. 16.6%; TT-homozygotes: 2.5 vs. 3.2%). The FSHB -211G -> T TT-genotype was strongly associated with elevated FSH (TT-homozygosity effect 2.05 U/liter, P = 0.003). LH increased with the number of T-alleles (1.30 U/liter per T-allele, P < 0.001). Additionally, FSHB -211G -> T was associated with reduced progesterone (-1.96 ng/ml per T-allele, P = 0.047). Conclusions: This is a report on phenotypic consequences of FSHB -211G -> T on the hypothalamic-pituitary-ovarian axis in women. The findings, partially contradictory to those in men, point to a gender-specific compensatory mechanism of gonadotropin secretion, probably involving progesterone. (J Clin Endocrinol Metab 98: E82-E86, 2013)

Serotonin is a biogenic monoamine conserved across phyla that is implicated in diverse physiological and behavioural functions. On examining the expression of the rate-limiting enzymes in serotonin synthesis, tryptophan hydroxylases (TPHs), in the teleost medaka (Oryzias latipes), we found that males have much higher levels oftph1expression as compared with females. This robust sexual dimorphism was found to probably result from the direct stimulation oftph1transcription by androgen/androgen receptor binding to canonical bipartite androgen-responsive elements in its proximal promoter region. Our results further revealed thattph1expression occurs exclusively in pro-opiomelanocortin (pomc)-expressing cells and that the resulting serotonin and its derivative melatonin inhibit the expression of the pituitary hormone genes,fshb,slandtshb. This suggests that serotonin and/or melatonin synthesized inpomc-expressing cells act in a paracrine manner to suppress pituitary hormone levels. Consistent with these findings and the male-biased expression oftph1, the expression levels offshb,slandtshbwere all higher in females than in males. Taken together, the male bias intph1expression and consequent serotonin/melatonin production presumably contribute to sex differences in the expression of pituitary hormones and ultimately in the physiological functions mediated by them.