Dyck P J, Zimmerman B R, Vilen T H, Minnerath S R, Karnes J L, Yao J K, Poduslo J F
Peripheral Nerve Laboratory, Mayo Clinic, Rochester, MN 55905.
N Engl J Med. 1988 Sep 1;319(9):542-8. doi: 10.1056/NEJM198809013190904.
We measured the alcohol sugars in sural nerves from 11 controls, 21 conventionally treated patients with diabetes and neuropathy, and 4 diabetics without neuropathy. The results were related to metabolic control and to clinical, neuropathological, and morphometric abnormalities in the nerves. The mean endoneurial glucose, fructose, and sorbitol values were higher in diabetic patients than in controls. Linear regression analysis revealed that nerve sorbitol content in the diabetics was inversely related to the number of myelinated fibers (P = 0.003). Mean nerve levels of myo-inositol were not decreased in the diabetic patients, with or without neuropathy, and were not associated with any of the neuropathological end points of diabetes. Our results indicate that myo-inositol deficiency is not part of the pathogenesis of human diabetic neuropathy, as had been hypothesized. Other accumulated alcohol sugars, however, were increased in diabetes and were associated with the severity of neuropathy. On repeat biopsy, six diabetics, treated for a year with the aldose reductase inhibitor sorbinil, had decreased endoneurial levels of sorbitol (P less than 0.01) and fructose (0.05 less than P less than 0.1), but unchanged levels of myo-inositol.
我们测定了11名对照者、21名接受传统治疗的糖尿病伴神经病变患者以及4名无神经病变的糖尿病患者腓肠神经中的醇糖。研究结果与代谢控制以及神经的临床、神经病理学和形态学异常相关。糖尿病患者神经内膜中的葡萄糖、果糖和山梨醇平均水平高于对照者。线性回归分析显示，糖尿病患者神经中的山梨醇含量与有髓纤维数量呈负相关（P = 0.003）。无论有无神经病变，糖尿病患者神经中的肌醇平均水平均未降低，且与糖尿病的任何神经病理学终点均无关联。我们的研究结果表明，正如之前所假设的那样，肌醇缺乏并非人类糖尿病神经病变发病机制的一部分。然而，其他累积的醇糖在糖尿病中有所增加，且与神经病变的严重程度相关。在重复活检时，6名接受醛糖还原酶抑制剂索比尼尔治疗一年的糖尿病患者，其神经内膜中山梨醇水平降低（P < 0.01），果糖水平降低（0.05 < P < 0.1），但肌醇水平未变。
