Shillabeer G, Chamoun C, Hatch G, Lau D C
Department of Medicine, University of Ottawa, ON, Canada.
Biochem Biophys Res Commun. 1995 Feb 15;207(2):768-74. doi: 10.1006/bbrc.1995.1253.
This study tested the hypothesis using cultured L6 myocytes that insulin resistance in muscle may be the consequence of triacylglycerol accretion in the tissue itself. Exposure of L6 myocytes to triacylglycerol for 4 hours resulted in significant transfer of lipid into the cells compared to control cells treated for only 5 min. Insulin-stimulated 2-deoxyglucose uptake in L6 myocytes was reduced when the cells were preloaded with triacylglycerol. Insulin-independent and insulin-stimulated 2-deoxyglucose uptake were inhibited by cytochalasin B, indicating that both were transporter-mediated. Diacylglycerol mimicked insulin action by increasing 2-deoxyglucose uptake and this was also reduced by triacylglycerol preloading, suggesting that the effect was not mediated at the insulin receptor. Thus, triacylglycerol may exert a direct effect on muscle cell insulin sensitivity possibly at the level of diacylglycerol second messenger pathway.
本研究使用培养的L6肌细胞验证了如下假设：肌肉中的胰岛素抵抗可能是组织自身三酰甘油积聚的结果。与仅处理5分钟的对照细胞相比，将L6肌细胞暴露于三酰甘油4小时导致脂质大量转移至细胞内。当细胞预先加载三酰甘油时，L6肌细胞中胰岛素刺激的2-脱氧葡萄糖摄取减少。细胞松弛素B抑制了非胰岛素依赖性和胰岛素刺激的2-脱氧葡萄糖摄取，表明二者均由转运体介导。二酰甘油通过增加2-脱氧葡萄糖摄取模拟胰岛素作用，而预先加载三酰甘油也降低了这种作用，这表明该效应不是在胰岛素受体水平介导的。因此，三酰甘油可能在二酰甘油第二信使途径水平对肌肉细胞胰岛素敏感性产生直接影响。
