Department of Medicine, Section of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, IL.
Department of Medicine, Section of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, IL.
J Nutr Biochem. 2019 May;67:90-100. doi: 10.1016/j.jnutbio.2019.01.020. Epub 2019 Feb 10.
Mixtures of the two major conjugated linoleic acid (CLA) isomers trans-10,cis-12-CLA and cis-9,trans-11-CLA are used as over the counter supplements for weight loss. Because of the reported adverse effects of CLA on insulin sensitivity in some mouse studies, we sought to compare the impact of dietary t10c12-CLA and c9t11-CLA on liver, adipose tissue, and systemic metabolism of adult lean mice. We fed 8 week-old C57Bl/6J male mice with low fat diets (10.5% Kcal from fat) containing 0.8% t10c12-CLA or c9t11-CLA for 9 or 38 days. Diets containing c9t11-CLA had minimal impact on the endpoints studied. However, 7 days after starting the t10c12-CLA diet, we observed a dramatic reduction in fat mass measured by NMR spectroscopy, which interestingly rebounded by 38 days. This rebound was apparently due to a massive accumulation of lipids in the liver, because adipose tissue depots were visually undetectable. Hepatic steatosis and the disappearance of adipose tissue after t10c12-CLA feeding was associated with elevated plasma insulin levels and insulin resistance, compared to mice fed a control diet or c9t11-CLA diet. Unexpectedly, despite being insulin resistant, mice fed t10c12-CLA had normal levels of blood glucose, without signs of impaired glucose clearance. Hepatic gene expression and fatty acid composition suggested enhanced hepatic de novo lipogenesis without an increase in expression of gluconeogenic genes. These data indicate that dietary t10c12-CLA may alter hepatic glucose and lipid metabolism indirectly, in response to the loss of adipose tissue in mice fed a low fat diet.
两种主要共轭亚油酸(CLA)异构体反式-10,顺式-12-CLA 和顺式-9,反式-11-CLA 的混合物被用作减肥的非处方补充剂。由于一些小鼠研究报告 CLA 对胰岛素敏感性有不良影响,我们试图比较饮食中 t10c12-CLA 和 c9t11-CLA 对成年瘦鼠肝脏、脂肪组织和全身代谢的影响。我们用低脂肪饮食(脂肪热量的 10.5%)喂养 8 周龄 C57Bl/6J 雄性小鼠,其中含有 0.8%的 t10c12-CLA 或 c9t11-CLA,持续 9 或 38 天。含 c9t11-CLA 的饮食对研究终点的影响最小。然而,在开始 t10c12-CLA 饮食的 7 天后,我们观察到通过 NMR 光谱测量的脂肪量急剧减少,有趣的是,到 38 天时又出现反弹。这种反弹显然是由于肝脏中脂质的大量积累,因为脂肪组织储库肉眼不可见。与喂食对照饮食或 c9t11-CLA 饮食的小鼠相比,t10c12-CLA 喂养后肝脏脂肪变性和脂肪组织消失与血浆胰岛素水平升高和胰岛素抵抗有关。出乎意料的是,尽管胰岛素抵抗,喂食 t10c12-CLA 的小鼠血糖水平正常,没有葡萄糖清除受损的迹象。肝基因表达和脂肪酸组成表明肝从头脂肪生成增强,而糖异生基因表达没有增加。这些数据表明,饮食中 t10c12-CLA 可能通过响应低脂肪饮食喂养的小鼠脂肪组织的丧失,间接改变肝脏的葡萄糖和脂质代谢。