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首页> 外文期刊>Nutrition Research >A long-term sucrose-rich diet increases diacylglycerol content and membrane nPKCO expression and alters glucose metabolism in skeletal muscle of rats
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A long-term sucrose-rich diet increases diacylglycerol content and membrane nPKCO expression and alters glucose metabolism in skeletal muscle of rats

机译:长期富含蔗糖的饮食可增加大鼠骨骼肌中二酰基甘油含量和膜nPKCO表达并改变葡萄糖代谢

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This study was designed to examine the possible metabolic pathways that could be involved in the increase of lipid storage in the gastrocnemius muscle and insulin resistance in rats fed a sucrose-rich diet (sucrose 63%, wt/wt) for 30 weeks. In the gastrocnemius muscle, malonyl-CoA, diacylglycerol (DAG), and long-chain acyl-CoA (LC ACoA) contents; novel protein kinase C 0 (nPKCt9) and Glut4 protein mass; and hexokinase, GSa, and pyruvate dehydrogenase (PDH) and PDH kinase activities were analyzed. Theresults were compared with age-matched rats fed a control diet (starch 63%, wt/wt) during the same period. In the sucrose-rich-fed rats, 2 major findings are reported: (1) a significant increase of DAG levels and nPKC0 protein mass in the membrane fraction, accompanied by a high increase of both triglycerides and LC ACoA contents in the gastrocnemius muscle; and (2) a significant decrease of hexokinase activity without changes of Glut4 protein mass and an altered glucose oxidation (low PDH complex andhigh PDH kinase activities). These findings suggest that different metabolic pathways could contribute to the development of insulin resistance in the skeletal muscle of long-term sucrose-fed rats: (1) a high level of LC ACoA by their esterification to DAG could stimulate the increase and translocation of the nPKCt9 isozyme to the cell membrane, which might interfere with insulin signaling pathways; (2) a decrease in the hexokinase activity alters glucose phosphorylation and could impair insulin-mediated glucose disposal; (3) a significant reduction of flux through PDH complex may limit glucose oxidation via the glucose-fatty acid cycle.
机译:这项研究的目的是研究喂食富含蔗糖饮食(蔗糖63%,wt / wt)达30周的大鼠腓肠肌中脂质存储量增加和胰岛素抵抗的可能代谢途径。在腓肠肌中,丙二酰辅酶A,二酰基甘油(DAG)和长链酰基辅酶A(LC ACoA)含量;新的蛋白激酶C 0(nPKCt9)和Glut4蛋白质量;分析了己糖激酶,GSa,丙酮酸脱氢酶(PDH)和PDH激酶的活性。将结果与在同一时期喂食对照饮食(淀粉63%,wt / wt)的年龄相匹配的大鼠进行比较。在富含蔗糖的大鼠中,有2个主要发现:(1)膜部分的DAG水平和nPKC0蛋白质量显着增加,同时腓肠肌中甘油三酸酯和LC ACoA含量均显着增加; (2)己糖激酶活性显着降低,而Glut4蛋白质量没有变化,并且葡萄糖氧化没有改变(PDH复合物低而PDH激酶活性高)。这些发现表明,不同的代谢途径可以促进长期蔗糖喂养的大鼠骨骼肌胰岛素抵抗的发展:(1)高水平的LC ACoA酯化为DAG可以刺激其增加和转运。细胞膜上存在nPKCt9同工酶,可能会干扰胰岛素信号通路; (2)己糖激酶活性的降低改变了葡萄糖的磷酸化,并可能损害胰岛素介导的葡萄糖处置; (3)通过PDH络合物的通量显着减少可能会限制通过葡萄糖-脂肪酸循环的葡萄糖氧化。

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