Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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

Science (New York, N.Y.) | Mar 30, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11283375

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 RIS Download

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

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIGMS NIH HHS, Id: GM19091

Mouse Genome Informatics (Data, Gene Annotation)

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.