A thorough understanding of the factors that regulate the secretion of FSH is critical for the development of efficient methods for fertility regulation. The purpose of this review is to evaluate what is currently known about the existence of FSH-releasing factor(s). It considers the obstacles encountered in understanding the control of FSH secretion, current knowledge of the nature of FSH secretion and the mechanisms involved in controlling FSH secretion, the arguments that have been posed against the need for an FSH-releasing factor and finally the evidence available to date supporting the existence of FSH-releasing factor(s).
V Padmanabhan and AS McNeilly
K. Leung, V. Padmanabhan, L. J. Spicer, H. A. Tucker, R. E. Short, and E. M. Convey
Summary. Thirty primiparous suckling beef cows were slaughtered on Day 7, 14, 28,42 or 56 after parturition. Some had resumed oestrous cyclicity by the time they were slaughtered on Days 42 and 56. Amongst acyclic cows between Days 7 and 42, pituitary LH concentrations and basal and GnRH-induced release of LH from pituitary explants doubled. Pituitary FSH concentration and basal release in FSH increased only by 15–20%, while GnRH-induced release of FSH in vitro was unchanged. During post-partum anoestrus, overall mean concentrations of serum FSH did not change, whereas overall mean concentrations and pulse amplitudes of serum LH increased. Numbers and affinity constants of GnRH-binding sites in pituitary glands remained constant during the post-partum period studied. We conclude that, under these experimental conditions, numbers and affinity constants of GnRH-binding sites in the pituitary gland of post-partum beef cows do not limit the ability of the anterior pituitary gland to release gonadotrophins.
E M Beckett, O Astapova, T L Steckler, A Veiga-Lopez, and V Padmanabhan
Gestational testosterone treatment causes maternal hyperinsulinemia, intrauterine growth retardation (IUGR), low birth weight, and adult reproductive and metabolic dysfunctions. Sheep models of IUGR demonstrate placental insufficiency as an underlying cause of IUGR. Placental compromise is probably the cause of fetal growth retardation in gestational testosterone-treated sheep. This study tested whether testosterone excess compromises placental differentiation by its androgenic action and/or via altered insulin sensitivity. A comparative approach of studying gestational testosterone (aromatizable androgen) against dihydrotestosterone (non-aromatizable androgen) or testosterone plus androgen antagonist, flutamide, was used to determine whether the effects of testosterone on placental differentiation were programed by its androgenic actions. Co-treatment of testosterone with the insulin sensitizer, rosiglitazone, was used to establish whether the effects of gestational testosterone on placentome differentiation involved compromised insulin sensitivity. Parallel cohorts of pregnant females were maintained for lambing and the birth weight of their offspring was recorded. Placental studies were conducted on days 65, 90, or 140 of gestation. Results indicated that i) gestational testosterone treatment advances placental differentiation, evident as early as day 65 of gestation, and culminates in low birth weight, ii) placental advancement is facilitated at least in part by androgenic actions of testosterone and is not a function of disrupted insulin homeostasis, and iii) placental advancement, while helping to increase placental efficiency, was insufficient to prevent IUGR and low-birth-weight female offspring. Findings from this study may be of relevance to women with polycystic ovary syndrome, whose reproductive and metabolic phenotype is captured by the gestational testosterone-treated offspring.