Leptin inhibits prehibernation hyperphagia and reduces body weight in arctic ground squirrels

Olav A. Ormseth, Margery Nicolson, Mary Ann Pelleymounter, Bert Boyer

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

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 3 wk via miniosmotic 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 after 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 3 wk 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume271
Issue number6 40-6
StatePublished - Dec 1 1996
Externally publishedYes

Fingerprint

Sciuridae
Hyperphagia
Leptin
Body Weight
Adiposity
Hormones
Electric Conductivity
Energy Metabolism
Adipose Tissue
Mammals
Eating

Keywords

  • adiposity
  • hibernating mammals
  • obesity
  • satiety

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Leptin inhibits prehibernation hyperphagia and reduces body weight in arctic ground squirrels. / Ormseth, Olav A.; Nicolson, Margery; Pelleymounter, Mary Ann; Boyer, Bert.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 271, No. 6 40-6, 01.12.1996.

Research output: Contribution to journalArticle

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