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O位N-乙酰葡糖胺(O-GlcNAc)修饰普遍存在于许多胞浆蛋白与核蛋白中,并且与磷酸化体系竞争相同的丝氨酸/苏氨酸残基位点,进而调节细胞内重要的生理过程。胰岛素抵抗是指胰岛素刺激肌肉和脂肪细胞摄取和利用葡萄糖的能力降低。高血糖能提高细胞内己糖胺通路的活性,使参与信号转导的蛋白质的O-GlcNAc修饰水平异常升高,打破了O-GlcNAc修饰与磷酸化的动态平衡,诱导胰岛素抵抗。本文就近年来有关O-GlcNAc修饰异常与胰岛素抵抗的相互关系做一综述。
O-position N-acetylglucosamine (O-GlcNAc) modifications are ubiquitous in many cytoplasmic proteins and nucleoproteins and compete with the phosphorylation system for the same serine / threonine residue sites to regulate intracellularly important Physiological process. Insulin resistance refers to the reduced ability of insulin to stimulate muscle and adipocyte uptake and utilization of glucose. Hyperglycemia can increase the activity of hexosamine channels in cells, which leads to abnormally high level of O-GlcNAc modification involved in signal transduction, breaking the homeostasis of O-GlcNAc modification and phosphorylation and inducing insulin resistance. This review summarizes the relationship between O-GlcNAc modification and insulin resistance in recent years.