βAR Signaling required for Diet-induced Thermogenesis And Obesity Resistance

摘要

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 hypoth- esis, we created mice that lack the three known βARs (β-less mice). β-less mice on a Chow diet had a educed 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.