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1 Gladstone Institute of Cardiovascular Disease, San Francisco 94103; and 2 Cardiovascular Research Institute and 3 Department of Medicine, University of California, San Francisco, California 94143
Mice lacking
acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), a
key enzyme in triglyceride synthesis, have increased energy expenditure and therefore are resistant to obesity. Because ambient temperature can significantly affect energy expenditure in mice, we
undertook these studies to determine the effects of different ambient
temperatures on energy expenditure, food intake, and thermoregulation in DGAT1-deficient [Dgat1(
/)] mice.
Dgat1(/) mice had increased energy expenditure
irrespective of changes in the ambient temperature. Although core
temperature was normal, surface temperature was increased in
Dgat1(/) mice, most likely reflecting an active mechanism to dissipate heat from increased thermogenesis.
Dgat1(/) mice had increased food intake at baseline, and
this hyperphagia became more pronounced upon exposure to cold. When
fasted in a cold environment, Dgat1(/) mice developed
hypothermia, which was associated with hypoglycemia. These results
suggest that the hyperphagia in Dgat1(/) mice is a
secondary mechanism that compensates for the increased utilization of
fuel substrates. Our findings offer insights into the mechanisms of
hyperphagia and increased energy expenditure in a murine model of
obesity resistance.
fasting; glycogen; hypoglycemia; thermoregulation; triglyceride synthesis; uncoupling protein 1; acyl-CoA:diacylglycerol acyltransferase 1
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