betaAR signaling required for diet-induced thermogenesis and obesity resistance

Eric S Bachman1, Harveen Dhillon, Chen-Yu Zhang

  • 1Department of Medicine, Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, 99 Brookline Avenue, Boston, MA 02215, USA.

Science (New York, N.Y.)
|August 6, 2002
PubMed

Insights

Beta-adrenergic receptors (betaARs) are crucial for preventing obesity. Mice lacking betaARs showed a failure in diet-induced thermogenesis, leading to massive obesity when fed a high-fat diet.

Area of Science:

  • Physiology
  • Metabolism
  • Obesity Research

Background:

  • The brain is thought to sense excessive caloric intake and activate thermogenesis to prevent obesity.
  • The sympathetic nervous system, via beta-adrenergic receptors (betaARs), is a potential efferent pathway for this homeostatic mechanism.

Purpose of the Study:

  • To investigate the necessity of beta-adrenergic receptors (betaARs) in diet-induced thermogenesis and obesity prevention.
  • To determine the role of the sympathetic nervous system in mediating the metabolic response to caloric intake.

Main Methods:

  • Generation of mice lacking the three known betaARs (beta-less mice).
  • Comparison of metabolic rate and obesity development between beta-less mice and wild-type mice on Chow and high-fat diets.

Main Results:

  • Beta-less mice exhibited a reduced metabolic rate and slight obesity on a standard diet.
  • On a high-fat diet, beta-less mice developed severe obesity, unlike wild-type controls.
  • This massive obesity in beta-less mice was attributed to a complete failure of diet-induced thermogenesis.

Conclusions:

  • Beta-adrenergic receptors (betaARs) are essential for diet-induced thermogenesis.
  • The betaAR-mediated sympathetic nervous system pathway is critical for defending against diet-induced obesity.

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