Mouse recombinant leptin inhibits prehibernation hyperphagia and
reduces body weight in arctic ground squirrels.
Ormseth, Olav A., Margery Nicolson[acute]a, Mary Ann
Pellymounter[acute]a, and Bert B. Boyer.
Institute of Arctic Biology, University of Alaska, Fairbanks,
Alaska 99775, Department of Immunology and Neurobiology, Amgen Inc.,
Thousand Oaks, California 91320
APStracts 3:0344R, 1996.
The ob gene product leptin is thought to play a physiological role in
the fine tuning of a homeostatic mechanism regulating satiety and
adiposity. Mouse recombinant leptin was administered to seasonally
hyperphagic arctic ground squirrels as a first step in demonstrating
the evolutionary conservation of leptin function and the potential
involvement of leptin in the seasonal regulation of adiposity in
hibernators. Continuous infusion of leptin for three weeks via mini
-osmotic pumps resulted in a reduction in food intake and body weight
in a manner consistent with its proposed role as a satiety hormone.
During the recovery period following leptin administration, squirrels
that had received leptin became hyperphagic relative to controls.
Percent body fat was estimated at weekly intervals by measuring total
body electrical conductivity and decreased after three weeks of
leptin administration. Our observations support the role of leptin as
a regulatory hormone involved in the control of satiety, adiposity
and possibly energy expenditure in hibernating mammals.
Received 27 June 1996; accepted in final form 26 August 1996.
APS Manuscript Number R374-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996