Regulation by oestradiol of serum levels of LH and FSH and pituitary levels of gonadotrophin-releasing hormone receptors after ovariectomy in the rat

Abstract

We studied cyclic and ovariectomized, oestradiol treated rats to investigate whether oestradiol concentrations before ovariectomy determine the dynamics of the rises in serum levels of LH and FSH, and in pituitary gonadotrophin-releasing hormone (GnRH) receptors after ovariectomy. In cyclic rats, ovariectomy on metoestrus (oestradiol = 44 pmol/l), but not at midnight of dioestrus (oestradiol = 254 pmol/l) was followed by a rise in GnRH receptors 40 h later. Randomly cyclic females were ovariectomized under ether anaesthesia and treated with s.c. oestradiol implants for 2 days to provide serum levels spanning the physiological range. Exposure to lower oestradiol concentrations (48 or 74 pmol/l) resulted in significant rises in levels of LH and FSH, and in GnRH receptors earlier than exposure to higher (148 or 309 pmol/l) oestradiol levels (2 compared with 4 days). GnRH given for 24 h after removal of the implant was unable to induce a rise in GnRH receptors in any group, while LH and FSH responses to GnRH were proportional to the pretreatment levels of oestradiol. This suggests that the concentration of oestradiol before ovariectomy determines the subsequent dynamics of LH and FSH and of GnRH receptors through actions at the hypothalamic and pituitary level.

Effects of Progesterone on Benzene Toxicity in Rats

“…Testosterone was found to be the main regulator in mice, whereas in rats this role seems to belong to oestradiol (24). In our experiments, benzene administration depleted progesterone in rats.…”

Genetically Determined Dosage of Follicle-Stimulating Hormone (FSH) Affects Male Reproductive Parameters

“…The data of the current study grouped the investigated male reproductive parameters into three categories: 1) sensitive to T-allele dosage (significant reduction in serum FSH, total testosterone, inhibin-B); 2) affected only among TT-homozygotes and most probably involving compensatory mechanisms to maintain wild-type levels in GT carriers (significantly decreased testes volume and increased serum LH; trend for lower sperm concentration); and 3) not affected by constitutively reduced FSH levels (serum SHBG and estradiol, sperm motility, and morphology). We propose that these observations may reflect not only the short-term effect of reduced circulating FSH on reproductive physiology of adult men, but also the past long-term effects of altered FSH concentration on developing gonads and on early reprogramming of hormonal balance due to shared regulatory and feedback loops with FSH (8, 15). During fetal, neonatal, and pubertal development, FSH activates the mitotic proliferation of the Sertoli and germ cells, and in the pubertal phase, FSH induces mitotic activity of the spermatogonia and regulates spermatogonial survival (16, 17).…”