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The role of thermoregulatory thermogenesis in the development of obesity in genetically-obese (ob/ob) mice pair-fed with lean siblings

Published online by Cambridge University Press:  09 March 2007

P. L. Thurlby
Affiliation:
Dunn Nutrition Laboratory, University of Cambridge and Medical Research Council, Milton Road, CambridgeCB4 1XJ
P. Trayhurn
Affiliation:
Dunn Nutrition Laboratory, University of Cambridge and Medical Research Council, Milton Road, CambridgeCB4 1XJ
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Abstract

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1. In order to quantitatively assess the energetic significance of reduced thermoregulatory thermogenesis in the accumulation of excess body fat in genetically-obese (ob/ob) mice experiments have been conducted at four environmental temperatures (17, 23, 28 and 33°) in which young growing obese animals were pair-fed for 10 d to the ad lib. intake of lean siblings.

2. The food intake of the lean mice increased with decreasing environmental temperature: at 17° the intake was 86% higher than that at 33°.

3. The estimated gain in carcass energy of lean mice rose with increasing temperature, from 82 kJ at 17° to 150 kJ at 33°. The energy gain of the pair-fed obese mice was higher than that of the lean at all temperatures but showed a slight decrease with increasing temperature, from 231 kJ at 17° to 191 kJ at 33°.

4. Environmental temperature affected the ‘excess’ energy gain of the obese mice. At 17° the obese mice deposited 182% more energy than the lean but this difference decreased progressively with increasing temperature to 127, 62 and 27% more energy at 23, 28 and 33° respectively.

5. At all environmental temperatures the pair-fed obese mice deposited considerably less protein than their lean controls. The deposition ranged from 32% (at 17°) to 56% (at 28°) of that of the lean mice.

6. It is concluded that environmental temperature plays a major role in determining the excess energy gain of ob/ob mice receiving the same amount of food as lean controls, and that the low energy expenditure and consequent high metabolic efficiency of this mutant is due primarily to reduced thermoregulatory thermogenesis.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1979

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