Evaluation of liver fatty acid oxidation in the leptin-deficient obese mouse.

Academic Article

Abstract

  • We hypothesized that liver fatty acid oxidation (FAO) is compromised in the leptin-deficient obese (Lep(ob)/Lep(ob)) mouse model, and that this would be further challenged when these mice were fed a high-fat diet. Obese mice had a 3.8-fold increased body fat content and a 9-fold increased liver fat content as compared to control mice when both groups were fed a low-fat diet. The expression of liver FAO enzymes, carnitine palmitoyltransferase-1a, long-chain acyl-CoA dehydrogenase, medium-chain acyl-CoA dehydrogenase, and short-chain acyl-CoA dehydrogenase, was not affected in obese mice as compared to controls on either a low-fat or a high-fat diet. The expression of very-long-chain acyl-CoA dehydrogenase was elevated in obese mice on the control diet, as compared to control mice. For all measures evaluated, increasing the level of fat in the diet had a smaller effect than leptin deficiency. In summary, despite obese mice having an excess of fat available for mitochondrial beta-oxidation in liver, overall energy balance appeared to dictate that the net liver FAO remained at control levels.
  • Published In

    Keywords

  • Acyl-CoA Dehydrogenase, Acyl-CoA Dehydrogenase, Long-Chain, Adipose Tissue, Analysis of Variance, Animals, Blotting, Northern, Blotting, Western, Body Weight, Carnitine O-Palmitoyltransferase, Dietary Fats, Fatty Acids, Female, Leptin, Lipids, Liver, Mice, Mice, Inbred C57BL, Mice, Obese, Obesity, Organ Size, Oxidation-Reduction, RNA, Messenger, Specific Pathogen-Free Organisms, Time Factors
  • Digital Object Identifier (doi)

    Author List

  • Brix AE; Elgavish A; Nagy TR; Gower BA; Rhead WJ; Wood PA
  • Start Page

  • 219
  • End Page

  • 226
  • Volume

  • 75
  • Issue

  • 3