AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 5 756-R762, Copyright © 1987 by American Physiological Society
Brown fat thermogenesis in a rat model of dietary obesity
J. S. Fisler, J. R. Lupien, R. D. Wood, G. A. Bray and R. A. Schemmel
Department of Medicine, School of Medicine, University of Southern California, Los Angeles 90033.
The effects of chronic feeding of a high-fat diet or a cafeteria-type diet
on weight gain and thermogenesis in brown adipose tissue as measured by the
binding of a purine nucleotide (guanosine 5'-diphosphate, GDP) to
mitochondria of brown adipose tissue have been studied in two strains of
rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats,
which are resistant to developing obesity when eating a high-fat diet or
drinking sucrose solutions, have greater specific GDP binding in
interscapular brown adipose tissue (IBAT) than do Osborne-Mendel rats,
which are sensitive to fat-induced obesity. A high-fat diet, fed
isoenergetically to the low-fat diet, did not increase the growth of IBAT
and decreased specific GDP binding in both strains. Feeding a cafeteria
diet resulted in obesity and increased mass and protein content of the IBAT
in both strains of rats. However, specific GDP binding increased in
response to cafeteria feeding only in the Osborne-Mendel rats. These
studies show that thermogenesis, as measured by GDP binding to mitochondria
in brown adipose tissue, is suppressed by both isoenergetic and ad libitum
feeding of a high-fat diet. The higher basal GDP binding in the brown fat
of the S 5B/Pl rats suggests that higher thermogenesis of this tissue
contributes to the resistance of this strain to fat-induced obesity. The
inability of S 5B/Pl rats to further increase thermogenesis when eating a
cafeteria diet may contribute to their becoming obese.
