Behavioral, endocrine and hypothalamic responses to involuntary
overfeeding.
Seeley, Randy J., Claire A. Matson, Mark Chavez, Stephen C. Woods,
Mary F. Dallman, Michael W. Schwartz.
Departments of Psychology and Medicine, University of Washington,
Department of Endocrinology and Metabolism, Seattle VA Medical
Center, Department of Physiology, University of California at San
Francisco
APStracts 3:0226R, 1996.
The suppression of food intake after a period of forced overfeeding is
potent and long lasting, yet little is known of the underlying
mechanisms for this regulatory response. Rats were overfed via a
surgically implanted gastrostomy tube. During overfeeding, plasma
insulin and corticotropin releasing hormone (CRH) mRNA in the
paraventricular nucleus of the hypothalamus were elevated compared to
controls and to overfed rats allowed three days to recover from the
overfeeding regimen such that body weight returned to the level of
controls. In contrast, rats that were not overfed but were pairfed to
the low spontaneous food intake of previously overfed rats lost
weight and had significantly reduced plasma insulin and elevated mRNA
for neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus.
The results indicate that overfeeding produces an activation of
hypothalamic CRH system that may contribute to the hypophagia that
accompanies involuntary overfeeding. Further, the hypothalamic NPY
response to food restriction is not tied to low food intake per se,
but rather to negative energy balance.
Received 18 April 1996; accepted in final form 24 May 1996.
APS Manuscript Number R220-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96