己醣胺、胰岛素抵抗和糖尿病的并发症:当前状态。

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己醣胺、胰岛素抵抗和糖尿病的并发症:当前状态。

是杂志性金属底座。2006年1月,290 (1):E1-E8。

PubMed ID

16339923 (在PubMed

]

文摘

己醣胺生物合成途径(HBP)是糖酵解的相对较小的分支。到转化为氨基葡萄糖- 6 -磷酸果糖6-phosphate,由第一和病原谷氨酰胺酶催化:fructose-6-phosphate amidotransferase (GFAT)。主要的最终产品是UDP-N-acetylglucosamine (UDP-GlcNAc)。连同其他HBP生成的氨基糖,它为糖基侧链提供了必要的构建模块,蛋白质和脂质。UDP-GlcNAc调节流量通过调节HBP GFAT活动和义务O-GlcNAc转移酶的底物。后者是胞质及核酶,催化一个可逆,转译后的蛋白质改性,转移在O-linkage GlcNAc (O-GlcNAc)到特定的丝氨酸/苏氨酸残基的蛋白质。代谢通量增加HBP的影响被认为是通过增加O-GlcNAcylation介导的。几个调查人员认为HBP函数作为细胞营养传感器和在发展的过程中发挥作用的胰岛素抵抗和血管并发症糖尿病。需要增加通量HBP和足够的一些代谢影响持续,葡萄糖通量增加,促进糖尿病并发症,例如,减少的表情肌浆网钙(2 +)在心肌细胞atp酶和感应及和纤溶酶原激活物inhibitor-1血管平滑肌细胞、系膜细胞和主动脉内皮细胞。机制与增强O-GlcNAcylation某些转录因子是相一致的。 The role of HBP in the development of insulin resistance has been controversial. There are numerous papers showing a correlation between increased flux through HBP and insulin resistance; however, the causal relationship has not been established. More recent experiments in mice overexpressing GFAT in muscle and adipose tissue or exclusively in fat cells suggest that the latter develop in vivo insulin resistance via cross talk between fat cells and muscle. Although the relationship between HBP and insulin resistance may be quite complex, it clearly deserves further study in concert with its role in the complications of diabetes.

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药物

葡萄糖胺