βAR Signaling Required for Diet-Induced Thermogenesis and Obesity Resistance

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Abstract
Excessive caloric intake is thought to be sensed by the brain, which then activates thermogenesis as a means of preventing obesity. The sympathetic nervous system, through β-adrenergic receptor (βAR) action on target tissues, is likely the efferent arm of this homeostatic mechanism. To test this hypothesis, we created mice that lack the three known βARs (β-less mice). β-less mice on a Chow diet had a reduced metabolic rate and were slightly obese. On a high-fat diet, β-less mice, in contrast to wild-type mice, developed massive obesity that was due entirely to a failure of diet-induced thermogenesis. These findings establish that βARs are necessary for diet-induced thermogenesis and that this efferent pathway plays a critical role in the body's defense against diet-induced obesity.