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Diabetes. 2005 Dec;54(12):3510-6.

Resistance to diet-induced obesity in mu-opioid receptor-deficient mice: evidence for a "thrifty gene".

Author information

1
Laboratoire Homéostasie-Allostasie-Pathologie, EA 3666, University of Bordeaux 2, 146 Rue Leo Saignat, 33076 Bordeaux, France. antoine.tabarin@chu-bordeaux.fr

Erratum in

  • Diabetes. 2006 Feb;55(2):563. Chaves, Yolanda Diz [corrected to Diz-Chaves, Y].
  • Diabetes. 2006 Mar;55(3):862.

Abstract

Using pharmacological tools, a role for opioid receptors in the regulation of food intake has been documented. However, the involvement of specific receptor subtypes remains questionable, and little information is available regarding a role for opioid receptors in energy metabolism. Using adult male mice lacking the mu-opioid receptor (MOR) gene (MOR-/-), we show that the MOR is not essential for the maintenance of normal levels of ad libitum food intake but does modulate the efficiency of energy storage during high-fat diets through the regulation of energy partitioning. When fed a regular diet, MOR-/- mice displayed only subtle alterations in energy homeostasis, suggesting a relative overuse of fat as a fuel source in the fed state. When fed a high-fat diet, MOR-/- mice were resistant to obesity and impaired glucose tolerance, despite having similar energy intake to wild-type mice. This resistance to obesity was associated with a strong induction of the expression of key mitochondrial enzymes involved in fatty acid oxidation within skeletal muscle. This metabolic role of the MOR, which is consistent with the properties of a "thrifty gene," suggests that the MOR pathway is a potential target for pharmacological intervention in the treatment of obesity associated with the intake of fatty diets.

PMID:
16306369
DOI:
10.2337/diabetes.54.12.3510
[Indexed for MEDLINE]
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