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Capsaicin desensitization induces atrophy of brown adipose tissue in rats.

作者信息

Cui J, Zaror-Behrens G, Himms-Hagen J

机构信息

Department of Biochemistry, University of Ottawa Faculty of Medicine, Ontario, Canada.

出版信息

Am J Physiol. 1990 Aug;259(2 Pt 2):R324-32. doi: 10.1152/ajpregu.1990.259.2.R324.

DOI:10.1152/ajpregu.1990.259.2.R324
PMID:2386244
Abstract

Interscapular brown adipose tissue (BAT) of capsaicin-desensitized (Cap-Des) rats is atrophied, having a lower wet weight, a reduced total protein content, and as little as 10% of the normal content of uncoupling protein (UCP). Because the mitochondrial concentration of UCP, relative to other mitochondrial proteins, is not altered in Cap-Des rats, it is concluded that most of the mitochondria of BAT of Cap-Des rats have been lost. Consistent with this interpretation is a reduction of almost 40% of the overall thermogenic response to infused norepinephrine by anesthetized Cap-Des rats. Feeding a palatable diet had a delayed thermogenic effect and no trophic effect on BAT of Cap-Des rats. Food selection and intake were normal in Cap-Des rats, and diet-induced weight gain was the same as in control rats. Exposure of Cap-Des rats to cold for 1 or 7 days exerted a normal thermogenic effect on BAT but a delayed trophic effect. The cold-induced increase in thyroxine 5'-deiodinase in BAT occurred normally. Cap-Des rats were hypothermic at 1 day but normothermic by 7 days of cold exposure. The concentration of thyroid hormones in their blood was normal. It is suggested that the depletion of sensory neuropeptides in BAT presumed to be brought about by Cap-Des results either in loss of a trophic influence on mitochondriogenesis in BAT or in lack of an inhibitory influence on mitochondrial breakdown in BAT and leads to atrophy of BAT in rats living at 26 degrees C and an impaired response to stimulation by diet.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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