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首页> 外文期刊>Journal of Cellular Physiology >Role of glycogen content in insulin resistance in human muscle cells.
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Role of glycogen content in insulin resistance in human muscle cells.

机译：糖原含量在胰岛素抵抗中的作用人类的肌肉细胞。

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摘要

We have used primary human muscle cell cultures to investigate the role of glycogen loading in cellular insulin resistance. Insulin pre-treatment for 2 h markedly impaired insulin signaling, as assessed by protein kinase B (PKB) phosphorylation. In contrast, insulin-dependent glycogen synthesis, glycogen synthase (GS) activation, and GS sites 3 de-phosphorylation were impaired only after 5 h of insulin pre-treatment, whereas 2-deoxyglucose transport was only decreased after 18 h pre-treatment. Insulin-resistant glycogen synthesis was associated closely with maximal glycogen loading. Both glucose limitation and 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) treatment during insulin pre-treatment curtailed glycogen accumulation, and concomitantly restored insulin-sensitive glycogen synthesis and GS activation, although GS de-phosphorylation and PKB phosphorylation remained impaired. Conversely, glycogen super-compensation diminished insulin-sensitive glycogen synthesis and GS activity. Insulin acutely promoted GS translocation to particulate subcellular fractions; this was abolished by insulin pre-treatment, as was GS dephosphorylation therein. Limiting glycogen accumulation during insulin pre-treatment re-instated GS dephosphorylation in particulate fractions, whereas glycogen super-compensation prevented insulin-stimulated GS translocation and dephosphorylation. Our data suggest that diminished insulin signaling alone is insufficient to impair glucose disposal, and indicate a role for glycogen accumulation in inducing insulin resistance in human muscle cells.
机译：我们使用的主要人类肌肉细胞培养糖原加载的作用进行调查细胞的胰岛素抵抗。预处理2 h明显受损的胰岛素信号,评估蛋白激酶B (PKB)磷酸化。糖原合成、糖原合成酶(GS)激活和GS站点3 de-phosphorylation只有5 h后受损的胰岛素吗预处理,而2-deoxyglucose运输只有18 h预处理后下降。胰岛素抵抗增强糖原合成是与最大糖原负荷密切相关。葡萄糖限制和5-aminoimidazole-4-carboxamide1-beta-D-ribofuranoside(爱卡)治疗期间胰岛素预处理减少糖原积累,与此同时恢复胰岛素敏感糖原合成和GS激活,尽管GS de-phosphorylation和PKB磷酸化仍然受损。相反,糖原super-compensation减少胰岛素敏感糖原合成和GS活性。易位,颗粒亚细胞分数;预处理,GS去磷酸化在其中。胰岛素预处理恢复GS脱磷酸作用在颗粒分数,而糖原super-compensation预防刺激GS易位和去磷酸化。减少胰岛素信号本身不足以损害葡萄糖处理,表明糖原累积的作用在人类肌肉诱导胰岛素抵抗细胞。

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