βAR signaling required for diet-induced thermogenesis and obesity resistance

Eric S. Bachman, Harveen Dhillon, Chen Yu Zhang, Saverio Cinti, Antonio C. Bianco, Brian K. Kobilka, Bradford B. Lowell

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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.

Original languageEnglish
Pages (from-to)843-845
Number of pages3
JournalScience
Volume297
Issue number5582
DOIs
StatePublished - Aug 2 2002

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Cite this

Bachman, E. S., Dhillon, H., Zhang, C. Y., Cinti, S., Bianco, A. C., Kobilka, B. K., & Lowell, B. B. (2002). βAR signaling required for diet-induced thermogenesis and obesity resistance. Science, 297(5582), 843-845. https://doi.org/10.1126/science.1073160