Animal models in the study of nutritional infertility

Abstract

To summarize the physiological bases of infertility during undernutrition. When energy expenditure consistently exceeds intake, survival receives temporary priority over fertility, and reproduction is deferred until conditions are more favorable. This nutritional infertility is due to inhibition of both gonadotropin-releasing hormone secretion and copulatory behaviors. Recent work has focused on the nature of the metabolic signals to the brain, detection of these signals, and the neural circuitry involved. This work is reviewed and summarized. It was once erroneously believed that female mammals had to maintain a particular body fat content to remain fertile. We now know that the primary metabolic factor is short-term availability of glucose and fatty acids for oxidation. Metabolic fuel availability is detected in the caudal hindbrain and possibly elsewhere. This information is relayed to the forebrain via projections containing catecholamines and neuropeptide-Y, where they activate corticotropin-releasing hormone neurons. Acting as a neurotransmitter, this hormone inhibits gonadotropin-releasing hormone secretion and estrous behavior. Conversely, corticotropin-releasing hormone antagonists reverse the effects of food deprivation on both measures, indicating that corticotropin-releasing hormone is vital in the nutritional suppression of reproduction. Leptin may modulate reproductive responses to changes in short-term fuel availability.