Date of Award

Spring 1987

Degree Type

Thesis - Restricted

Degree Name

Master of Science (MS)



First Advisor

Piacsek, Bela

Second Advisor

Horseman, Nelson

Third Advisor

Vomachka, Archie


A reduction in food intake to 60% of normal daily consumption results in a significant delay in puberty. Several possible mechanisms have been proposed to account for this disruption in reproductive function: the hypothalamus may have an increased sensitivity to the inhibitory effect of estrogen; there may be a deficiency in gonadotropin releasing hormone (GnRH) from the hypothalamus; or the sensitivity of the pituitary to GnRH is decreased. All three proposed mechanisms may account for the reduced LH levels found with underfeeding thus not allowing an LH surge which necessarily precedes ovulation. This work has been directed toward elucidating the possible change in sensitivity at the level of the pituitary. In order to test the sensitivity of the pituitary, immature female rats were ovariectomized (OVX) and subsequently treated with estradiol benzoate (EB) and progesterone (P) to suppress the endogenous gonadotropin hypersecretion response. Seven days after ovx, animals were challenged intravenously with various doses of GnRH. Results of the dose-response studies show significantly reduced serum LH concentrations in response to high doses of GnRH in reduced fed (R) animals when compared to control ad libitum fed animals (C). In contrast to this reduced response, at low GnRH doses, R rats had significantly higher serum LH concentrations than controls. These results suggest that reduced food intake alters pituitary LH release in response to GnRH in prepubertal female rats. In addition, data indicate that the time course of LH release seems to be GnRH dose dependent. Furthermore, EB plus progesterone treatment can influence the effect of reduced food intake on GnRH induced LH release since serum LH concentrations of OVX/EB and OVX/EB+P treated animals differed following identical GnRH doses.