Zhou Xiao-Rong, Sun Chang-Hao, Liu Jia-Ren, Zhao Dan
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China.
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China; Department of Food Science, Cornell University, Stocking Hall, Ithaca, NY 14853-7201, USA.
Growth Horm IGF Res. 2008 Oct;18(5):361-368. doi: 10.1016/j.ghir.2008.01.001. Epub 2008 Mar 4.
Conjugated linoleic acid (CLA) is a class of positional, geometric, conjugated dienoic isomers of linoleic acid. Dietary CLA supplementation has resulted in a dramatic decrease in body fat mass in mice. However, some but not all studies in mice and humans have found that CLA promoted insulin resistance, and there were conflicting reports on the effects of CLA on peroxisomal proliferator-activated receptor-gamma (PPAR gamma) activation and expression. The objective of present study was to investigate the effect of CLA on insulin resistance and its molecular mechanisms. Fifty male Wistar rats were randomly designed to the control, high-fat and high-fat with CLA (0.75, 1.50, and 3.00 g in per 100 g diet) groups. The effect of CLA on insulin sensitivity and the mechanism of resisting diabetes by CLA were investigated by RT-PCR assay. The results showed that supplementation with CLA significantly reduced body weight gain and white fat pad weight in the rats, the levels of plasma free fatty acids (FFA), triglycerides (TGs), cholesterin (TC), leptin, insulin and blood glucose concentration in the obese rats of CLA group were also decreased compared to the rats in the high-fat group. Dietary CLA increased the mRNA expression of PPAR gamma, fatty acid binding proteins (aP2), fatty acid transporter protein (FATP), acyl-CoA synthetase (ACS) and adiponectin in the adipose tissues of obese rats. The results suggest that CLA may ameliorate insulin resistance by activating PPAR gamma, and increasing the expression of PPAR gamma target genes such as ap2, FATP, FAT, and adiponectin in the white adipose tissue.
共轭亚油酸（CLA）是一类亚油酸的位置、几何和共轭二烯异构体。膳食补充CLA已导致小鼠体内脂肪量显著减少。然而，一些但并非所有关于小鼠和人类的研究发现CLA会促进胰岛素抵抗，并且关于CLA对过氧化物酶体增殖物激活受体γ（PPARγ）激活和表达的影响存在相互矛盾的报道。本研究的目的是探讨CLA对胰岛素抵抗的影响及其分子机制。将50只雄性Wistar大鼠随机分为对照组、高脂组和高脂添加CLA组（每100克饮食中分别添加0.75、1.50和3.00克CLA）。通过RT-PCR分析研究CLA对胰岛素敏感性的影响以及CLA抵抗糖尿病的机制。结果表明，补充CLA可显著降低大鼠体重增加和白色脂肪垫重量，与高脂组大鼠相比，CLA组肥胖大鼠的血浆游离脂肪酸（FFA）、甘油三酯（TGs）、胆固醇（TC）、瘦素、胰岛素和血糖浓度水平也有所降低。膳食CLA增加了肥胖大鼠脂肪组织中PPARγ、脂肪酸结合蛋白（aP2）、脂肪酸转运蛋白（FATP）、酰基辅酶A合成酶（ACS）和脂联素的mRNA表达。结果表明，CLA可能通过激活PPARγ并增加白色脂肪组织中PPARγ靶基因如ap2、FATP、FAT和脂联素的表达来改善胰岛素抵抗。
