Abstract
The mechanism by which mice, exposed to the cold, mobilize endogenous or exogenous fuel sources for heat production is unknown. To address this issue we carried out experiments using 3 models of obesity in mice: C57BL/6J+/+ (wild-type B6) mice with variable susceptibility to obesity in response to being fed a high-fat diet (HFD), B6. Ucp1-/- mice with variable diet-induced obesity (DIO) and a deficiency in brown fat thermogenesis and B6. Lep-/- with defects in thermogenesis, fat mobilization and hyperphagia. Mice were exposed to the cold and monitored for changes in food intake and body composition to determine their energy balance phenotype. Upon cold exposure wild-type B6 and Ucp1-/- mice with diet-induced obesity burned endogenous fat in direct proportion to their fat reserves and changes in food intake were inversely related to fat mass, whereas leptin-deficient and lean wild-type B6 mice fed a chow diet depended on increased food intake to fuel thermogenesis. Analysis of gene expression in the hypothalamus to uncover a central regulatory mechanism revealed suppression of the Npvf gene in a manner that depends on the reduced ambient temperature and degree of exposure to the cold, but not on adiposity, leptin levels, food intake or functional brown fat.
Highlights
IntroductionIts long-term effectiveness as a strategy to reduce obesity has been questioned because of the expectation that increased energy expenditure for the cold environment will increase food intake, thereby neutralizing the weight reducing effects of the cool environment [1], a skepticism associated with the effectiveness of physical activity as an anti-obesity strategy [2]
Reduced ambient temperature will increase thermogenesis and reduce obesity
We show that upon cold exposure lean mice maintain body composition but increase food intake to fuel thermogenesis, whereas cold-exposed mice with diet-induced obesity (DIO) utilize endogenous fat stores and transition to increased food intake as body composition approaches that of the lean controls
Summary
Its long-term effectiveness as a strategy to reduce obesity has been questioned because of the expectation that increased energy expenditure for the cold environment will increase food intake, thereby neutralizing the weight reducing effects of the cool environment [1], a skepticism associated with the effectiveness of physical activity as an anti-obesity strategy [2]. This skepticism emerges from the adipostat hypothesis itself, which predicts that reductions in fat mass by cold stimulation will be compensated by increased food intake to maintain its adiposity index [3]. When an individual is exposed to a cold environment how the physiological decision is made to use endogenous energy reserves or to increase food intake and how this decision is influenced by the obese state of the individual is unknown
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