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 beta-adrenergic receptor (betaAR) 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 betaARs (beta-less mice). beta-less mice on a Chow diet had a reduced metabolic rate and were slightly obese. On a high-fat diet, beta-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 betaARs are necessary for diet-induced thermogenesis and that this efferent pathway plays a critical role in the body's defense against diet-induced obesity.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adipose Tissue, Brown / drug effects
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Adipose Tissue, Brown / metabolism
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Animals
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Basal Metabolism / drug effects
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Body Temperature / drug effects
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Body Weight / drug effects
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Body Weight / genetics
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Diet*
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Dietary Fats / administration & dosage
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Dietary Fats / pharmacology
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Energy Intake
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Female
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Homeostasis / drug effects
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Immunohistochemistry
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Male
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Mice
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Mice, Knockout
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Obesity / blood
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Obesity / genetics
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Obesity / metabolism*
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Obesity / prevention & control
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Oxygen Consumption / drug effects
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Phenotype
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Receptors, Adrenergic, beta / genetics
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Receptors, Adrenergic, beta / metabolism*
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Signal Transduction* / drug effects
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Sympathetic Nervous System / drug effects
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Sympathetic Nervous System / physiology
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Thermogenesis / genetics
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Thermogenesis / physiology*
Substances
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Dietary Fats
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Receptors, Adrenergic, beta