Greene D A, Lattimer S A, Sima A A
Diabetes Research and Training Center, University of Michigan, Ann Arbor 48109.
Diabetes. 1988 Jun;37(6):688-93. doi: 10.2337/diab.37.6.688.
Alterations in myo-inositol and phosphoinositide metabolism, induced by hyperglycemia and prevented by aldose reductase inhibitors, are implicated in impaired Na+-K+-ATPase regulation in peripheral nerve and other tissues prone to diabetic complications by an increasing range of scientific observations. However, the precise role of these related metabolic derangements in various stages of clinical complications is complex. For instance, it appears that these biochemical defects may play a role not only in the initiation of diabetic neuropathy but also in its later progression. Therefore, full appreciation of the potential pathogenetic role of altered phosphoinositide metabolism in diabetic complications requires detailed studies of both the earliest and the more mature stages of these disease processes.
越来越多的科学观察表明，高血糖诱导的、醛糖还原酶抑制剂可预防的肌醇和磷酸肌醇代谢改变，与外周神经及其他易患糖尿病并发症的组织中钠钾ATP酶调节常调节调节受损有关。然而，这些相关代谢紊乱在临床并发症各阶段的确切作用很复杂。例如，这些生化缺陷似乎不仅在糖尿病神经病变的起始阶段起作用，还在其后期进展中起作用。因此，要充分认识磷酸肌醇代谢改变在糖尿病并发症中的潜在致病作用，需要对这些疾病过程的最早阶段和更成熟阶段进行详细研究。
