Suppression of LH secretion in food-restricted lactating females: effects of ovariectomy and bromocryptine treatment

Abstract

It has been shown that restricting food in lactating rats for the first 2 weeks postpartum at a level of 60% of the ad-libitum daily ration increases the length of lactational dioestrus by about 7 days but little is known about correlated changes in hormone levels. In the first experiment we report changes in LH, prolactin (PRL) and ACTH secretion in food-restricted and ad-libitum fed lactating rats at various stages of lactation. Our results demonstrate that food restriction during the first 2 weeks of lactation did not affect PRL or ACTH secretion, but decreased plasma LH levels despite comparable GnRH receptor density between food-restricted and ad-libitum fed females. In the second experiments we investigated a possible causal relationship between the increased secretion of progesterone seen in food-restricted females and the suppression of plasma LH levels, by determining the effects of bromocryptine treatment and ovariectomy on LH secretion in both ad-libitum fed and food-restricted lactating females. LH suppression in food-restricted lactating females was not affected by ovariectomy or bromocryptine treatment, although the latter treatment significantly increased GnRH receptor number. These data suggest that factors other than ovarian steroids, PRL or increased adrenocortical activity modulate LH secretion and the length of lactational dioestrus in food-restricted lactating females.

Food restriction during lactation suppresses Kiss1 mRNA expression and kisspeptin-stimulated LH release in rats

“…In the present study, we used a model in which food restriction for the first 2 weeks of lactation delays the resumption of LH secretion and the estrous cycle, allowing a comparison of changes in Kiss1 mRNA at the same stage during lactation, but either before or after the resumption of cycles. As has been reported previously, food-restricted dams in the present study had increased progesterone concentrations and decreased leptin concentrations and had not resumed estrous cyclicity by day 20 pp, demonstrating the consistency of this model (Woodside 1991, Walker et al 1995, Abizaid et al 2004. The results of the present study demonstrate that prolonged lactational diestrus induced by food restriction for the first 2 weeks of lactation is associated with a reduction in AVPV Kiss1 mRNA expression and a decrease in kisspeptin-induced secretion of LH on day 15 pp compared with that in AL-fed lactating dams.…”

“…As weaning approaches, basal LH concentrations begin to increase (Walker et al 1995) and the ability of estrogen to invoke a LH surge gradually returns (Abizaid et al 2003). In the present study, we used a model in which food restriction for the first 2 weeks of lactation delays the resumption of LH secretion and the estrous cycle, allowing a comparison of changes in Kiss1 mRNA at the same stage during lactation, but either before or after the resumption of cycles.…”

“…Thus, dams in the foodrestricted group tested on day 20 pp had experienced 5 days of ad libitum access to food. Daily food rations were given to the food-restricted dams at w0900 h. This food restriction paradigm predictably extends the period of lactational diestrus by w1 week (Woodside 1991, Walker et al 1995, Abizaid et al 2003, allowing investigation of the HPG axis before and after reactivation at the end of lactation.…”

“…It has been shown previously in rats that this period of lactational anovulation is accompanied by a suppression of pulsatile release of luteinizing hormone (LH; Smith 1978, Walker et al 1995 and a reduction in the ability of estrogen to stimulate a LH surge (Smith & Neill 1977, Smith 1978. Lactation is also associated with a huge metabolic demand due to the production of milk, and despite food consumption of w300% of that of virgin rats, lactating dams enter a state of negative energy balance.…”

“…In this model, food is returned ad libitum from day 15 of lactation onwards, yet the effects of this period of food restriction on the hypothalamic-pituitary-gonadal (HPG) axis persist after refeeding. In association with the prolonged period of lactational anovulation, pulsatile LH release remains suppressed for longer than is observed in ad libitum (AL)-fed dams (Woodside 1991, Walker et al 1995, and there is a delay in the restoration of estrogen's ability to induce a LH surge (Abizaid et al 2003). Overall, the foodrestricted dams experience a predictable and consistent delay in return to normal functioning of their HPG axis and the resumption of estrous cyclicity compared with the AL-fed dams, providing a useful model to investigate the mechanisms underlying the resumption of fertility after lactation.…”