Leptin increases uncoupling protein expression and energy
expenditure.
Scarpace, Philip J., Michael Matheny, Brad H. Pollock, and Nihal
T[umlaut]umer.
Geriatric Research, Education and Clinical Center, Department of
Veterans Affairs Medical Center, Gainesville, Florida 32608-1197, and
Department of Pharmacology and Therapeutics, Department of Health
Policy and Epidemiology, University of Florida College of Medicine,
Gainesville, Florida 32610
APStracts 4:0085E, 1997.
In ob/ob mice, leptin increases energy expenditure and sympathetic
outflow to brown adipose tissue (BAT). To test whether the mechanism
of increased energy expenditure may involve increased thermogenesis
in BAT, we acclimated normal rats to thermoneutrality for two weeks
followed by leptin administration for one week. Some rats were food
restricted for one week to the level of food consumption in the
leptin-treated ad libitum-fed rats, and the same rats were both food
restricted and administered leptin for a second week. We examined
oxygen consumption and uncoupling protein (UCP) expression in BAT.
Leptin increased oxygen consumption after the fifth and sixth day in
ad libitum-fed rats and after the fourth, fifth and sixth day in
food-restricted rats. Leptin increased BAT UCP mRNA levels greater
than two-fold in both ad libitum-fed and food-restricted rats. These
data demonstrate a leptin-induced increase in energy expenditure in
non-mutant rodents and suggest that one mechanism by which leptin
increases energy expenditure is through increased thermogenesis in
BAT, including increased expression of UCP.
Received 1 November 1996; accepted in final form 13 February
1997.
APS Manuscript Number E551-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 April 1997