Greene D A, Mackway A M
Diabetes. 1986 Oct;35(10):1106-8. doi: 10.2337/diab.35.10.1106.
Decreased sciatic nerve myo-inositol content and Na+-K+-ATPase activity have been associated with slowing of motor nerve conduction in the acutely diabetic rat and have been invoked as possible pathogenic factors in diabetic peripheral neuropathy. Aldose reductase inhibitors prevent these abnormalities in peripheral nerves of the streptozocin (STZ)-diabetic rat. Whether an analogous biochemical abnormality occurs in the autonomic nervous system and plays a role in the development of diabetic autonomic dysfunction is unknown. Therefore we examined the effect of 8 wk of untreated STZ diabetes and administration of 20 mg X kg-1 X day-1 of the aldose reductase inhibitor sorbinil on myo-inositol level and Na+-K+-ATPase activity in rat superior cervical ganglia. Both myo-inositol concentration and Na+-K+-ATPase activity were reduced in ganglia from untreated STZ-diabetic rats, and sorbinil administration prevented these abnormalities. Thus, a sorbinil-responsive metabolic defect involving myotional abnormalities in the somatic and autonomic nervous systems in diabetes.
在急性糖尿病大鼠中，坐骨神经肌醇含量降低和钠钾ATP酶活性降低与运动神经传导减慢有关，并被认为是糖尿病周围神经病变可能的致病因素。醛糖还原酶抑制剂可预防链脲佐菌素（STZ）糖尿病大鼠周围神经的这些异常。自主神经系统是否会出现类似的生化异常并在糖尿病自主神经功能障碍的发展中起作用尚不清楚。因此，我们研究了8周未治疗的STZ糖尿病以及给予20 mg·kg⁻¹·d⁻¹的醛糖还原酶抑制剂索比尼尔对大鼠颈上神经节中肌醇水平和钠钾ATP酶活性的影响。未治疗的STZ糖尿病大鼠神经节中的肌醇浓度和钠钾ATP酶活性均降低，而给予索比尼尔可预防这些异常。因此，糖尿病中存在一种对索比尼尔有反应的代谢缺陷，涉及躯体和自主神经系统的肌醇异常。
