Brown fat is essential for cold-induced thermogenesis but not for
obesity resistance in ap2-ucp mice.
Stefl, Bohum[acute]ir, Alena Janovsk[acute]a, Zden[grave]ik Hodny,
Martin Rossmeisl, Milada Hor[acute]akov[acute]a, Ivo Syrovy,
Jaroslava B[acute]emov[acute]a, B[grave]ila Bendlov[acute]a, and Jan
Kopecky.
Faculty of Sciences, Charles University; Institute of
Endocrinology; and Institute of Physiology, Academy of Sciences of
the Czech Republic; Prague, Czech Republic
APStracts 4:0258E, 1997.
The role of brown adipose tissue in total energy balance and cold
-induced thermogenesis was studied. Mice expressing mitochondrial
uncoupling protein 1 (UCP1) from the fat-specific aP2 gene promoter
(heterozygous and homozygous aP2-Ucp transgenic mice), and their
nontrasgenic C57BL6/J littermates were used. The transgenic animals
are resistant to obesity induced by a high fat diet, presumably due
to ectopic synthesis of UCP1 in white fat. These animals exhibited
atrophy of brown adipose tissue, as indicated by smaller size of
brown fat and reduction of its total UCP1 and DNA contents.
Norepinephrine-induced respiration (measured in pentobarbital
-anesthetized animals) was decreased proportionally to the dosage of
the transgene, and the homozygous (but not heterozygous) transgenic
mice exhibited a reduction in their capacity to maintain body
temperature in the cold. Our results indicate that the role of brown
fat in cold-induced thermogenesis cannot be substituted by increased
energy expenditure in other tissues.
Received 24 September 1997; accepted in final form 12 November
1997.
APS Manuscript Number E448-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 12 December 1997