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Defective thermoregulatory thermogenesis does not cause onset of obesity in Zucker rats.

作者信息

Kaul R, Heldmaier G, Schmidt I

机构信息

W. G. Kerckhoff Institut, Max-Planck Institut für Physiologische und klinische Forschung, Bad Nauheim, Federal Republic of Germany.

出版信息

Am J Physiol. 1990 Jul;259(1 Pt 1):E11-8. doi: 10.1152/ajpendo.1990.259.1.E11.

Abstract

To test whether or not the onset of obesity in fatty (fa/fa) Zucker rats is caused by decreased thermoregulatory thermogenesis, pups were artificially reared above their lower critical temperature from 3 or 4 days of age. Littermates were continuously fed identical amounts of synthetic rat milk while body temperature (Tc) and oxygen consumption rate (VO2) were continuously recorded. When the daily mean Tc of all pups was held greater than 37 degrees C, neither Tc nor VO2 differed between fa/fa and genetically lean (Fa/-) pups during the first 2 wk of life. Tc and VO2 were significantly elevated in Fa/- pups during the third postnatal week. At both 16 and 21 days of age, fa/fa pups were identified by their low Tc during a brief cold exposure. Body fat and fat-free dry mass of fa/fa and Fa/- littermates differed at 21 but not at 16 days of age. The excess energy deposited as fat was partly derived from decreased nonthermoregulatory energy expenditure and decreased synthesis of lean body mass. Calculations support the speculation that a greater extraction of energy from the synthetic diet additionally supports the excess fat deposition. Decreased thermoregulatory thermogenesis and excess fat storage appear to be secondary and independent consequences of the primary genetic lesion.

摘要

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