Effect of nutrition on the balance of production of ovarian and pituitary hormones in ewes

Abstract Nutrition-induced changes in liveweight can induce changes in ovarian function and ovulation rate. This study was designed to test the hypothesis that heavy ewes are able to maintain similar concentrations of follicle-stimulating hormone (FSH) to light ewes through a loss of responsiveness to ovarian negative feedback. This hypothesis leads to the prediction that administration of ovarian hormones on the basis of metabolic body weight would result in the same gonadotrophin (FSH) concentrations in light and heavy ovariectomised ewes. We therefore examined the ovarian content of oestradiol and inhibin, and the FSH response to administration of these ovarian hormones in acutely ovariectomised heavy and light Merino ewes produced by differential feeding. At ovariectomy, follicular fluid was aspirated from the 6 largest follicles in each ewe and assayed for oestradiol and inhibin. Six days later, blood was sampled every 6 h for 2 days. Ewes were then given two subcutaneous progesterone implants and injected subcutaneously every 6 h for 5 days with oestradiol (37.4 ng kg −0.75 ) and charcoal-stripped bovine follicular fluid (0.04 ml kg −0.75 ). Blood was sampled before each injection and the plasma was assayed for FSH and inhibin. Oestradiol and its receptors were assayed in uterine tissue. Nutrition-induced increases in liveweight led to increases in the number of oestrogenic, potentially ovulatory ovarian follicles and the total ovarian content of oestradiol and inhibin. In the uterus, more oestradiol receptors and a higher oestradiol uptake were observed in light than in heavy ewes. After ovariectomy, FSH concentrations were inversely related to liveweight. However, when the ewes were treated with doses of ovarian hormones that were proportional to liveweight, the slope of the decline in FSH concentrations was independent of liveweight. We conclude that nutrition alters the balance between pituitary FSH secretion and gonadal feedback by changing the responsiveness to the inhibitory effects of oestradiol and inhibin.