Warren J M, Simon V A, Bartolini G, Erickson K L, Mackey B E, Kelley D S
Western Human Nutrition Research Center, ARS, USDA, and Department of Nutrition, University of California, Davis, California 95616, USA.
Lipids. 2003 May;38(5):497-504. doi: 10.1007/s11745-003-1090-0.
Although consumption of CLA mixtures has been associated with several health effects, less is known about the actions of specific CLA isomers. There is evidence that the t10,c12-CLA isomer is associated with alterations in body and organ weights in animals fed CLA, but the mechanisms leading to these changes are unclear. The purpose of this study was to determine the effects of two commonly occurring isomers of CLA on body composition and the transcription of genes associated with lipid metabolism. Eight-week-old female mice (n = 11 or 12/group) were fed either a control diet or diets supplemented with 0.5% c9,t11-CLA or t10,c12-CLA isomers or 0.2% of the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist fenofibrate for 8 wk. Body and retroperitoneal adipose tissue weights were significantly lower (6-10 and 50%, respectively), and liver weights were significantly greater (100%) in the t10,c12-CLA and the fenofibrate groups compared with those in the control group; body and tissue weights in the c9,t11-CLA group did not differ from those in the control group. Livers from animals in the t10,c12-CLA group contained five times more lipids than in the control group, whereas the lipid content of the fenofibrate group did not differ from that in the control group. Although fenofibrate increased the mRNA for PPARalpha, t10,c12-CLA decreased it. These results suggest that PPARalpha did not mediate the effects of t10,c12-CLA on body composition. The CLA isomers and fenofibrate altered mRNA levels for several proteins involved in lipid metabolism, but the most striking difference was the reduction of mRNA for leptin and adiponectin in the t10,c12-CLA group. These initial results suggest that changes associated with energy homeostasis and insulin action may mediate the effects of t10,c12-CLA on lipid metabolism.
尽管共轭亚油酸(CLA)混合物的摄入与多种健康效应相关,但对于特定CLA异构体的作用了解较少。有证据表明,t10,c12-CLA异构体与喂食CLA的动物的体重和器官重量变化有关,但导致这些变化的机制尚不清楚。本研究的目的是确定两种常见的CLA异构体对身体成分以及与脂质代谢相关基因转录的影响。将8周龄雌性小鼠(每组n = 11或12只)喂食对照饮食或补充0.5% c9,t11-CLA或t10,c12-CLA异构体的饮食,或0.2%的过氧化物酶体增殖物激活受体α(PPARα)激动剂非诺贝特,持续8周。与对照组相比,t10,c12-CLA组和非诺贝特组的体重和腹膜后脂肪组织重量显著降低(分别为6 - 10%和50%),肝脏重量显著增加(100%);c9,t11-CLA组的体重和组织重量与对照组无差异。t10,c12-CLA组动物的肝脏脂质含量是对照组的五倍,而非诺贝特组的脂质含量与对照组无差异。尽管非诺贝特增加了PPARα的mRNA水平,但t10,c12-CLA降低了它。这些结果表明,PPARα并未介导t10,c12-CLA对身体成分的影响。CLA异构体和非诺贝特改变了几种参与脂质代谢的蛋白质的mRNA水平,但最显著的差异是t10,c12-CLA组中瘦素和脂联素的mRNA减少。这些初步结果表明,与能量稳态和胰岛素作用相关的变化可能介导了t10,c12-CLA对脂质代谢的影响。