Effects of three different conjugated linoleic acid preparations on insulin signalling, fat oxidation and mitochondrial function in rats fed a high-fat diet.
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.
Choi
Joo Sun
JS
Division of Metabolic Diseases, Center for Biomedical Sciences, National Institute of Health, 194 Tongillo, Eunpyeong-gu, Seoul, 122-701, Korea.
Koh
In-Uk
IU
Jung
Myeong Ho
MH
Song
Jihyun
J
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
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