Attenuation of leptin-mediated effects by monosodium glutamate ( msg)-induced arcuate nucleus damage. Dawson, Ralph, Mary Ann Pelleymounter, William J. Millard, Steve Liu, and Baerbel Eppler. Department of Pharmacodynamics, College of Pharmacy, JHMHC Box 100487, University of Florida, Gainesville, FL 32610, and Department of Neurobiology, Amgen, Inc., 1840 DeHavilland Drive, Thousand Oaks, CA 91320
APStracts 4:0071E, 1997.
Leptin is a protein secreted by adipocytes that is important in regulating appetite and adiposity. Recent studies have suggested the presence of leptin receptors in the arcuate nucleus of the hypothalamus (ANH). Neonatal administration of MSG damages the ANH resulting in obesity and neuroendocrine dysfunction. Neonatal administration of MSG was utilized in order to test the hypothesis that the anatomical site for many of leptin's actions is the ANH. Female control (n=6) and MSG-treated rats (n=7) were implanted for 14 days with osmotic minipumps containing phosphate buffered saline (PBS) or leptin (1 mg/kg/day). Leptin suppressed (p < 0.05) body weight gain in controls, but did not suppress weight gain in MSG-treated rats. Leptin decreased (p < 0.05) fat depots in controls, but had no effect in MSG-treated rats. Night feeding was suppressed (p < 0.05) in leptin-treated control rats. MSG -treated rats showed a suppression in food intake that was of a smaller magnitude and appeared later in the course of leptin treatment. These findings suggest that leptin mediates some physiological actions related to fat mobilization via receptors located in the ANH.

Received 12 October 1996; accepted in final form 14 March 1997.
APS Manuscript Number E519-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 3 April 1997