Purushotham Aparna, Shrode Gayle E, Wendel Angela A, Liu Li-Fen, Belury Martha A
Department of Human Nutrition, The Ohio State University, Columbus, OH 43210, USA.
J Nutr Biochem. 2007 Oct;18(10):676-84. doi: 10.1016/j.jnutbio.2006.10.008. Epub 2007 Mar 21.
The dietary fatty acid conjugated linoleic acid (CLA) reduces hepatic lipid accumulation in some rodent models for obesity and hepatic steatosis. However, these effects are variable and complex due to differences in isomer responses and degree and sensitivity to changes in adiposity. Here, we hypothesized that CLA decreases hepatic steatosis in a diet-induced model of obesity in rats which are resistant to the adipose-lowering effects of CLA. To investigate this, we fed male Wistar rats a high-fat (20%) diet for 4 weeks to induce obesity and hepatic steatosis followed by low-fat (6.5%) experimental diets containing either 6.5% soybean oil (CON) or 1.5% CLA triglyceride mix plus 5% soybean oil (CLA). Dietary CLA significantly lowered hepatic triglycerides without changing weight, adiposity or adipokines, and was associated with significantly lower hepatic fatty acid synthase and stearoyl CoA desaturase-1 (SCD-1) mRNA levels and SCD-1 index along with significantly lower sterol regulatory element binding protein-1 mRNA, a transcription factor that regulates lipogenesis. Furthermore, the lower lipogenesis was associated with significantly higher mRNA expression of lipid oxidation gene peroxisome proliferator-activated receptor-alpha and acetyl CoA oxidase in the livers of rats fed dietary CLA. The lipid-lowering effects of CLA in the liver were observed in the absence of changes in adipose tissue and body weight. Thus, we conclude that in the Wistar rat model, where adipose levels remain static after feeding dietary CLA, hepatic lipid accumulation is reduced and these effects are not due to an improvement in overall adiposity.
膳食脂肪酸共轭亚油酸(CLA)在一些肥胖和肝脂肪变性的啮齿动物模型中可减少肝脏脂质蓄积。然而,由于异构体反应、肥胖程度及对肥胖变化的敏感性存在差异,这些作用具有变异性且较为复杂。在此,我们推测CLA可减轻饮食诱导的大鼠肥胖模型中的肝脂肪变性,这些大鼠对CLA的减脂作用具有抗性。为探究这一点,我们给雄性Wistar大鼠喂食高脂(20%)饮食4周以诱导肥胖和肝脂肪变性,随后喂食低脂(6.5%)实验饮食,其中一组含6.5%大豆油(CON),另一组含1.5%CLA甘油三酯混合物加5%大豆油(CLA)。膳食CLA显著降低了肝脏甘油三酯水平,而体重、肥胖程度或脂肪因子未发生变化,且与肝脏脂肪酸合酶和硬脂酰辅酶A去饱和酶-1(SCD-1)的mRNA水平及SCD-1指数显著降低相关,同时与甾醇调节元件结合蛋白-1的mRNA显著降低相关,该蛋白是一种调节脂肪生成的转录因子。此外,较低的脂肪生成与喂食CLA饮食的大鼠肝脏中脂质氧化基因过氧化物酶体增殖物激活受体-α和乙酰辅酶A氧化酶的mRNA表达显著升高相关。在脂肪组织和体重未发生变化的情况下,观察到了CLA对肝脏的降脂作用。因此,我们得出结论,在Wistar大鼠模型中,喂食CLA后脂肪水平保持稳定,肝脏脂质蓄积减少,且这些作用并非由于总体肥胖状况的改善。