Control of fertility by metabolic cues.
Wade, George N., Jill E. Schneider, Hui-Yun Li.
Department of Psychology and Neuroscience and Behavior Program, Box
37710, University of Massachusetts, Amherst, MA 01003-7710, USA,
Department of Biological Sciences, Lehigh University, 111 Research
Drive, Bethlehem, PA 18015, USA, The Salk Institute for Biological
Studies, P.O. Box 85800, San Diego, CA 92186-5800, USA
APStracts 2:0200E, 1995.
In female mammals, reproduction is extremely sensitive to the
availability of oxidizable metabolic fuels. When food intake is
limited or when an inordinate fraction of the available energy is
diverted to other uses such as exercise or fattening, reproductive
attempts are suspended in favor of processes necessary for individual
survival. Both reproductive physiology and sexual behaviors are
influenced by food availability. Nutritional effects on reproductive
physiology are mediated by changes in the activity of gonadotropin
-releasing hormone (GnRH) neurons in the forebrain, whereas the
suppression of sexual behaviors appears to be due, at least in part,
to decreases in estrogen receptor in the ventromedial hypothalamus.
Work using pharmacological inhibitors of glucose and fatty acid
oxidation indicates that reproductive physiology and behavior respond
to short-term (minute-to-minute or hour-to-hour) changes in metabolic
fuel oxidation, rather than to any aspect of body size or composition
(e.g., body fat content or fat-to-lean ratio). These metabolic cues
seem to be detected in the viscera (most likely in the liver) and in
the caudal hindbrain (probably in the area postrema). This metabolic
information is then transmitted to the GnRH-secreting or estradiol
-binding effector neurons in the forebrain. There is no evidence to
date for direct detection of metabolic cues by these forebrain
effector neurons. This metabolic fuels hypothesis is consistent with
a large body of evidence and seems to account for the infertility
that is seen in a number of situations, including famine, eating
disorders, excessive exercise, cold exposure, lactation, some types
of obesity, and poorly controlled diabetes mellitus.
Received 2 August 1995; accepted in final form 28 September 1995.
APS Manuscript Number E363-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95