Document Detail


Effects of three different conjugated linoleic acid preparations on insulin signalling, fat oxidation and mitochondrial function in rats fed a high-fat diet.
MedLine Citation:
PMID:  17408517     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Joo Sun Choi; In-Uk Koh; Myeong Ho Jung; Jihyun Song
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-04-04
Journal Detail:
Title:  The British journal of nutrition     Volume:  98     ISSN:  0007-1145     ISO Abbreviation:  Br. J. Nutr.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-12     Completed Date:  2007-09-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372547     Medline TA:  Br J Nutr     Country:  England    
Other Details:
Languages:  eng     Pagination:  264-75     Citation Subset:  IM    
Affiliation:
Division of Metabolic Diseases, Center for Biomedical Sciences, National Institute of Health, 194 Tongillo, Eunpyeong-gu, Seoul, 122-701, Korea.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Dietary Fats / administration & dosage*
Electron Transport Complex IV / metabolism
Energy Metabolism / genetics
Fatty Acids / genetics,  metabolism*
Insulin / metabolism*
Insulin Resistance / physiology
Linoleic Acids, Conjugated / administration & dosage*
Male
Mitochondria / drug effects,  enzymology,  metabolism*
Oxidation-Reduction / drug effects
PPAR alpha / metabolism
RNA, Messenger / analysis
Rats
Rats, Sprague-Dawley
Receptors, Adiponectin
Receptors, Cell Surface / blood
Signal Transduction / drug effects
Succinate Dehydrogenase / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Dietary Fats; 0/Fatty Acids; 0/Linoleic Acids, Conjugated; 0/PPAR alpha; 0/RNA, Messenger; 0/Receptors, Adiponectin; 0/Receptors, Cell Surface; 0/adiponectin receptor 1, rat; 0/adiponectin receptor 2, rat; 11061-68-0/Insulin; EC 1.3.99.1/Succinate Dehydrogenase; EC 1.9.3.1/Electron Transport Complex IV

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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