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Conjugated linoleic acid reduces visceral and ectopic lipid accumulation and insulin resistance in chronic severe hypertriacylglycerolemia

H. Malinska, M. Hüttl, O. Oliyarnyk, M. Bratova, L. Kazdova,

. 2015 ; 31 (7-8) : 1045-51. [pub] 20150420

Language English Country United States

Document type Journal Article, Research Support, Non-U.S. Gov't

E-resources Online Full text

NLK ProQuest Central from 2003-01-01 to 2 months ago
Medline Complete (EBSCOhost) from 2012-09-01 to 2015-07-31
Nursing & Allied Health Database (ProQuest) from 2003-01-01 to 2 months ago
Health & Medicine (ProQuest) from 2003-01-01 to 2 months ago
Health Management Database (ProQuest) from 2003-01-01 to 2 months ago
Public Health Database (ProQuest) from 2003-01-01 to 2 months ago

OBJECTIVE: The metabolic health effects of conjugated linoleic acid (CLA), which is one of the principal polyunsaturated fatty acids, are controversial and still not fully accepted. The aim of this study was to examine the effects of CLA on adiposity, ectopic lipid accumulation, and insulin-resistant states in a metabolic syndrome model of non-obese hereditary rats with hypertriacylglycerolmia (HHTg). METHODS: Groups of adult male HHTg rats were fed a high-carbohydrate diet (70% sucrose) with a 2% mixture of CLA isomers, or with the same amount of sunflower oil (control group) for 2 mo. RESULTS: CLA supplementation decreased body weight gain (P < 0.05) and visceral adipose tissue weight (P < 0.01), and distinctively reduced serum triacylglycerols (P < 0.01) and triacylglycerol accumulation in the liver, heart, muscle, and aorta. CLA-treated rats exhibited increased insulin sensitivity in the adipose (P < 0.01), a higher release of fatty acids (P < 0.001), and increased adiponectin secretion (P < 0.01).In the skeletal muscle, CLA supplementation was associated with increased glucose oxidation (P < 0.01) and an elevated anti-inflammatory index (P < 0.05), according to phospholipid fatty acid composition. In the liver, CLA reduced the oxidized form of glutathione and elevated the activity of glutathione-dependent antioxidant enzymes. CONCLUSION: Results suggest that CLA supplementation may protect against HHTg-induced dyslipidemia, ectopic lipid deposition, and insulin resistance. Increased glucose oxidation in the skeletal muscle as well as adiponectin secretion may play a role in the mechanism of the CLA action. Results suggest that CLA could reduce the negative consequences of HHTg and metabolic syndrome.

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