Alteration of 20:5n-3 and 22:6n-3 fat contents and liver peroxisomal activities in fenofibrate-treated rainbow trout.

Fish easily accumulate n-3 PUFA of exogenous origin, but the underlying mechanisms are not well established in the whole animal. This study was undertaken to investigate whether this feature was physiologically associated with mitochondrial and peroxisomal capacities that differentially affect FA oxidation. For this purpose, peroxisomal FA oxidation was increased by treating rainbow trout with fenofibrate, which strongly stimulates the peroxisome proliferator-activated receptor-a in rodents. Diets containing EPA and DHA, with or without fenofibrate added, were administered to male trout for 12 d. After treatment, neither liver hypertrophy nor accumulation of fat was apparent within the liver and muscle cells. However, fenofibrate treatment decreased the contents of EPA and DHA in the liver, white muscle, and intraperitoneal fat tissue, which represented (per whole body) at least 280 mg less than in controls. Carnitine-dependent palmitate oxidation rates, expressed per gram of liver, were slightly increased by fenofibrate when measured from tissue homogenates and were unchanged when calculated from isolated mitochondria, relative to control fish. The treatment altered neither carnitine palmitoyltransferase I activity rates, expressed per gram of liver, nor the sensitivity of the enzyme to malonyl-CoA inhibition, but did increase the malonyl-CoA content (+45%). Meanwhile, fenofibrate increased (by about 30%) the peroxisome-related activities, i.e., catalase, carnitine-independent palmitate oxidation, acyl-CoA oxidase, and the peroxisomal FA-oxidizing system, relative to the control group. The data strongly suggest that the induction of peroxisomal activities, some of which being able to oxidize very long chain FA, was responsible for the lower contents of EPA and DHA in the body lipids of fenofibrate-treated trout.