title: Effects of three different conjugated linoleic acid preparations on insulin signalling, fat oxidation and mitochondrial function in rats fed a high-fat diet.
abstract: To investigate the effects of three different conjugated linoleic acid (CLA) preparations containing different ratios of CLA isomers on insulin signalling, fatty acid oxidation and mitochondrial function, Sprague-Dawley rats were fed a high-fat diet either unsupplemented or supplemented with one of three CLA preparations at 1 % of the diet for 8 weeks. The first CLA preparation contained approximately 30 % cis-9, trans-11 (c9, t11)-CLA isomer and 40 % trans-10, cis-12 (t10, c12)-CLA isomer (CLA-mix). The other two preparations were an 80:20 mix (c9, t11-CLA-mix) or a 10:90 mix of two CLA isomers (t10, c12-CLA-mix). Insulin resistance was decreased in all three supplemented groups based on the results of homeostasis model assessment and the revised quantitative insulin-sensitivity check index. The phosphorylation of insulin receptor substrate-1 on serine decreased in the livers of all three supplemented groups, while subsequent Akt phosphorylation increased only in the t10, c12-CLA-mix group. Both the c9, t11-CLA-mix and the t10, c12-CLA-mix increased the expression of hepatic adiponectin receptors R1 and 2, which are thought to enhance insulin sensitivity and fat oxidation. The c9, t11-CLA-mix increased protein and mRNA levels of PPAR alpha, acyl-CoA oxidase and uncoupling protein, which are involved in fatty acid oxidation and energy dissipation. The c9, t11-CLA-mix enhanced mitochondrial function and protection against oxidative stress by increasing the activities of cytochrome c oxidase, manganese-superoxide dismutase, glutathione peroxidase, and glutathione reductase and the level of GSH. In conclusion, all three CLA preparations reduced insulin resistance. Among them, the c9, t11-CLA-mix was the most effective based on the parameters reflecting insulin resistance and fat oxidation, and mitochondrial antioxidative enzyme activity in the liver.
authors.affiliation: Division of Metabolic Diseases, Center for Biomedical Sciences, National Institute of Health, 194 Tongillo, Eunpyeong-gu, Seoul, 122-701, Korea.
authors.forename: Joo Sun
authors.initials: JS
authors.lastname: Choi
authors.forename: In-Uk
authors.initials: IU
authors.lastname: Koh
authors.forename: Myeong Ho
authors.initials: MH
authors.lastname: Jung
authors.forename: Jihyun
authors.initials: J
authors.lastname: Song
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage*; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000235:genetics; D005227:Fatty Acids / Q000235:genetics / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D044243:Linoleic Acids, Conjugated / Q000008:administration & dosage*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D047493:PPAR alpha / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface / Q000097:blood; D015398:Signal Transduction / Q000187:drug effects; D013385:Succinate Dehydrogenase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004041:Dietary Fats; D005227:Fatty Acids; D007328:Insulin; D044243:Linoleic Acids, Conjugated; D047493:PPAR alpha; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface; C504339:adiponectin receptor 1, rat; C506573:adiponectin receptor 2, rat; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV