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Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2.

Malonyl-coenzyme A (malonyl-CoA), generated by acetyl-CoA carboxylases ACC1 and ACC2, is a key metabolite in the regulation of energy homeostasis. Here, we show that Acc2-/- mutant mice have a normal life span, a higher fatty acid oxidation rate, and lower amounts of fat. In comparison to the wild type, Acc2-deficient mice had 10- and 30-fold lower levels of malonyl-CoA in heart and muscle, respectively. The fatty acid oxidation rate in the soleus muscle of the Acc2-/- mice was 30% higher than that of wild-type mice and was not affected by addition of insulin; however, addition of insulin to the wild-type muscle reduced fatty acid oxidation by 45%. The mutant mice accumulated 50% less fat in their adipose tissue than did wild-type mice. These results raise the possibility that pharmacological manipulation of ACC2 may lead to loss of body fat in the context of normal caloric intake.

Pubmed ID: 11283375

Authors

  • Abu-Elheiga L
  • Matzuk MM
  • Abo-Hashema KA
  • Wakil SJ

Journal

Science (New York, N.Y.)

Publication Data

March 30, 2001

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM19091

Mesh Terms

  • 3-Hydroxybutyric Acid
  • Acetyl-CoA Carboxylase
  • Adipose Tissue
  • Animals
  • Blood Glucose
  • Body Weight
  • Cholesterol
  • Energy Intake
  • Fasting
  • Fatty Acids
  • Female
  • Gene Targeting
  • Insulin
  • Lipid Metabolism
  • Liver
  • Liver Glycogen
  • Malonyl Coenzyme A
  • Mice
  • Mitochondria, Liver
  • Muscle, Skeletal
  • Mutation
  • Myocardium
  • Oxidation-Reduction
  • Palmitic Acid
  • Triglycerides
  • Weight Gain