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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Decreased muscle glucose transport/phosphorylation is an early defect in the pathogenesis of non-insulin-dependent diabetes mellitus.
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Decreased muscle glucose transport/phosphorylation is an early defect in the pathogenesis of non-insulin-dependent diabetes mellitus.

机译：肌肉葡萄糖转运/磷酸化水平降低是非胰岛素依赖型糖尿病发病机制中的早期缺陷。

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Recent studies have demonstrated that reduced insulin-stimulated muscle glycogen synthesis is the major cause of insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). This reduced rate has been assigned to a defect in either glucose transport or hexokinase activity. However it is unknown whether this is a primary or acquired defect in the pathogenesis of NIDDM. To examine this question, we measured the rate of muscle glycogen synthesis and the muscle glucose 6-phosphate (G6P) concentration using 13C and 31P NMR spectroscopy as well as oxidative and nonoxidative glucose metabolism in six lean, normoglycemic offspring of parents with NIDDM and seven age/weight-matched control subjects under hyperglycemic (approximately 11 mM)-hyperinsulinemic (approximately 480 pM) clamp conditions. The offspring of parents with NIDDM had a 50% reduction in total glucose metabolism, primarily due to a decrease in the nonoxidative component. The rate of muscle glycogen synthesis was reduced by 70% (P < 0.005) and muscle G6P concentration was reduced by 40% (P < 0.003), which suggests impaired muscle glucose transport/hexokinase activity. These changes were similar to those previously observed in subjects with fully developed NIDDM. When the control subjects were studied at similar insulin levels (approximately 440 pM) but euglycemic plasma glucose concentration (approximately 5 mM), both the rate of glycogen synthesis and the G6P concentration were reduced to values similar to the offspring of parents with NIDDM. We conclude that insulin-resistant offspring of parents with NIDDM have reduced nonoxidative glucose metabolism and muscle glycogen synthesis secondary to a defect in muscle glucose transport/hexokinase activity prior to the onset of overt hyperglycemia. The presence of this defect in these subjects suggests that it may be the primary factor in the pathogenesis of NIDDM.
机译：最近的研究表明，非胰岛素依赖型糖尿病（NIDDM）患者的胰岛素刺激性肌糖原合成减少是胰岛素抵抗的主要原因。该降低的速率已被归因于葡萄糖转运或己糖激酶活性的缺陷。然而，尚不清楚这是NIDDM发病机制的主要缺陷还是后天缺陷。为了检验这个问题，我们使用13C和31P NMR光谱法测量了6名NIDDM父母的瘦正常血糖后代中的肌肉糖原合成速率和6-磷酸葡萄糖葡萄糖（G6P）的浓度，以及氧化和非氧化葡萄糖代谢高血糖（约11 mM）-高胰岛素（约480 pM）钳制条件下年龄/体重匹配的对照受试者。 NIDDM父母的后代的总葡萄糖代谢降低了50％，这主要是由于非氧化成分的减少所致。肌肉糖原合成速率降低了70％（P <0.005），肌肉G6P浓度降低了40％（P <0.003），表明肌肉葡萄糖转运/己糖激酶活性受损。这些变化与先前在完全发展的NIDDM患者中观察到的变化相似。当对照受试者在相似的胰岛素水平（约440 pM）但正常血糖水平的血糖浓度（约5 mM）下进行研究时，糖原合成速率和G6P浓度均降低至与NIDDM父母的后代相似的值。我们得出结论，患有NIDDM的父母的胰岛素抵抗性后代降低了非氧化性葡萄糖代谢和肌肉糖原合成，继之于明显的高血糖发作之前，继发于肌肉葡萄糖转运/己糖激酶活性缺陷。在这些受试者中该缺陷的存在表明它可能是NIDDM发病机理中的主要因素。

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