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|Aquaculture Journal Articles
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|Conjugated Linoleic Acid Affects Lipid Composition, Metabolism, and Gene Expression in Gilthead Sea Bream (Sparus aurata L)
Calduch-Giner, Josep A
Vega-Rubin de Celis, Silvia
Tocher, Douglas R
Bautista, Jose M
|gilthead sea bream
Fishe Feeding and feeds
|Diez A, Menoyo D, Perez-Benavente S, Calduch-Giner JA, Vega-Rubin de Celis S, Obach A, Favre-Krey L, Boukouvala E, Leaver M, Tocher DR, Perez-Sanchez J, Krey G & Bautista JM (2007) Conjugated Linoleic Acid Affects Lipid Composition, Metabolism, and Gene Expression in Gilthead Sea Bream (Sparus aurata L). Journal of Nutrition, 137 (6), pp. 1363-1369. http://jn.nutrition.org/content/137/6/1363.abstract
|To maximize growth, farmed fish are fed high-fat diets, yet this can lead to high tissue lipid concentrations with impacts on quality. Given that intake of conjugated linoleic acid (CLA) reduces body fat in mammals, this study determines the effects of dietary CLA on growth, composition and postprandial metabolic variables in sea bream. Fish were fed three diets containing 48 g/100g protein and 24 g/100g fat including fish oil supplemented with 0 (control), 2 or 4% CLA for 12 wk. Feed intake and growth were lower in fish fed the CLA diets compared to controls. Feed efficiency was greater in fish fed the 2% CLA diet and total body fat was lower for the CLA diets versus controls. Circulating growth hormone remained unchanged but somatolactin levels were lower in CLA-fed fish. Tissue fatty acid composition changes were related to lower hepatic fatty acyl desaturase and elongase mRNA levels in fish fed CLA. Liver triglyceride levels were higher in fish fed 4% CLA and muscle levels were lower in fish fed both CLA diets versus controls. Most metabolic differences between controls and CLA-fed fish occurs at 6h but not at 24h after the last meal. These included lower postprandial circulating triglyceride concentrations, greater hepatic acyl-CoA-oxidase and lower L-3-hydroxyacyl-CoA dehydrogenase activities, as markers of peroxisomal and mitochondrial β-oxidation respectively, in CLA-fed fish. Our data suggest that CLA intake channels dietary lipid away from adipose tissue to liver, and a switch from hepatic mitochondrial to peroxisomal β-oxidation, possibly as a detoxification response.
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