trans-10,cis-12 Conjugated Linoleic Acid Enhances Endurance Capacity by Increasing Fatty Acid Oxidation and Reducing Glycogen Utilization in Mice

被引:30
|
作者
Kim, Jun Ho [1 ]
Kim, Jonggun [1 ]
Park, Yeonhwa [1 ]
机构
[1] Univ Massachusetts, Dept Food Sci, Amherst, MA 01003 USA
基金
美国食品与农业研究所;
关键词
Conjugated linoleic acid; Exercise; Fat oxidation; Endurance; Mice; BODY-COMPOSITION; EXERCISE ENDURANCE; ENERGY-METABOLISM; GENE-EXPRESSION; CREATINE MONOHYDRATE; INSULIN-RESISTANCE; SKELETAL-MUSCLE; LIPID OXIDATION; BETA-OXIDATION; SERUM LEPTIN;
D O I
10.1007/s11745-012-3698-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The supplementation of conjugated linoleic acid (CLA) has been shown to improve endurance by enhancing fat oxidation during exercise in rodents and humans. This study was designed to investigate the isomer-specific effects of CLA on endurance capacity and energy metabolism in mice during exercise. Male 129Sv/J mice were divided into three dietary groups and fed treatment diet for 6 weeks; control, 0.5 % cis-9,trans-11 (c9,t11) CLA, or 0.5 % trans-10,cis-12 (t10,c12) CLA. Dietary t10,c12 CLA induced a significant increase in maximum running time and distance until exhaustion with a dramatic reduction of total adipose depots compared to a control group, but there were no significant changes in endurance with the c9,t11 CLA treatment. Serum triacylglycerol and non-esterified fatty acid concentrations were significantly lower in the t10,c12 fed mice after exercise compared to control and the c9,t11 CLA fed-animals. Glycogen contents in livers of the t10,c12 fed-mice were higher than those in control mice, concomitant with reduction of serum l-lactate level. There were no differences in non-exercise physical activity among all treatment groups. In addition, the mRNA expression levels of carnitine palmitoyl transferase 1 beta, uncoupling protein 2 and peroxisome proliferator-activated receptor delta (PPAR delta) in skeletal muscle during exercise were significantly up-regulated by the t10,c12 CLA but not the c9,t11 CLA. These results suggest that the t10,c12 CLA is responsible for improving endurance exercise capacity by promoting fat oxidation with a reduction of the consumption of stored liver glycogen, potentially mediated via PPAR delta dependent mechanisms.
引用
收藏
页码:855 / 863
页数:9
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