Abstract

Prolonged restriction of dietary energy delays onset of puberty, disrupts cyclicity in sexually mature animals, and lengthens the postpartum anestrous period in domestic ruminants. One important mechanism by which energy restriction impairs reproductive activity seems to be suppression of the increase in LH pulse frequency that is necessary for growth of ovarian follicles to the preovulatory stage. Under-nutrition apparently inhibits pulsatile secretion of LH by reducing LHRH secretion by the hypothalamus. The ability of an animal to sustain a high-frequency mode of pulsatile LH release is related to its metabolic status. Mechanisms linking metabolic status to LHRH secretion have not been fully characterized. Changes in body fat have been associated with changes in reproductive activity, but it is unlikely that body fat per se regulates LHRH secretion. It is possible that pulsatile LHRH release is regulated by specific metabolites and(or) metabolic hormones that reflect nutritional status. Alternatively, availability of oxidizable metabolic fuels, such as glucose and nonesterified fatty acids, may influence activity of neurons that control LHRH release. Our understanding of how the central nervous system transduces information about nutritional status into neuroendocrine signals that control reproduction in cattle and sheep is limited by a lack of information concerning the nature of neurons controlling LHRH release in these species.

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