| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1975840 | Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology | 2009 | 7 Pages |
To explore the mechanisms leading to excessive adiposity in chicken, we investigated the regulation of fatty acid oxidation depending on genotype-related body fatness and diet composition. mRNA expression and/or activity of proteins involved in mitochondrial energy metabolism were measured in liver and gastrocnemius muscle of genetically lean or fat chickens reared on a low-fat/high-protein diet or an isoenergetic high-fat/low-protein diet (HF/LP). Muscle expressions of the muscle isoform of carnitine-palmitoyltransferase 1 (M-CPT1) and PPARβ/δ were higher in fat than in lean chickens. This was also observed in liver, although only with the HF/LP diet for M-CPT1. This could stimulate mitochondrial fatty acid oxidation in fat chickens. Up-regulations of liver and muscle CPT-1 hepatic isoform, and muscle cytochrome-c-oxidase mRNA expressions, and of β-hydroxyacyl-CoA-dehydrogenase activities suggest higher fatty acid utilization with the HF/LP diet. PPARβ/δ and PGC-1α could control fatty acid oxidation in muscle and liver, respectively. Regulation of avian uncoupling protein (avUCP) mRNA was tissue-dependent. Predominantly expressed in muscle, it was stimulated in fat and in HF/LP-fed chickens, where it could be associated to the special need in muscle anti-oxidant pathways of fatter animals. In liver it was lower in fat than in lean chickens, and its potential function remains to be clarified.
