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,
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 &LT; 0.05)
body weight gain in controls, but did not suppress weight gain in
MSG-treated rats. Leptin decreased (p &LT; 0.05) fat depots in
controls, but had no effect in MSG-treated rats. Night feeding was
suppressed (p &LT; 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