Calcutt N A, Tomlinson D R, Willars G B
Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham, U.K.
Life Sci. 1988;42(16):1515-20. doi: 10.1016/0024-3205(88)90008-2.
Ouabain-sensitive ATPase activity (expressed as nmol ADP produced/h/mg (wet) nerve +/- SEM) was measured in homogenates of sciatic nerve from control rats and rats with streptozotocin-induced diabetes of 8 wk duration. Nerves from diabetic rats showed activity (21.7 +/- 2.0) which was significantly (p less than 0.05) less than that of controls (34.6 +/- 4.8). These animals also showed a deficit in conduction velocity (m/sec +/- SEM) of sciatic nerve motoneurones (50.7 +/- 0.4 vs. 57.7 +/- 0.7 in controls; p less than 0.001). In parallel, matched control and diabetic groups were treated daily with mixed gangliosides extracted from bovine brain (10 mg/kg i.p.). After such treatment for 8 wk the deficit in ouabain-sensitive ATPase activity did not develop in the diabetic group (treated diabetics, 31.9 +/- 3.7; treated controls, 34.5 +/- 3.8). However, the treatment did not affect the deficit in motor nerve conduction velocity (treated diabetics, 50.9 +/- 1.1 vs. treated controls, 57.9 +/- 0.5; p less than 0.001). Accumulations of the polyol pathway metabolites--sorbitol and fructose--together with depletion of nerve myo-inositol were similar in both diabetic groups. These data indicate an etiology for the conduction velocity deficit which differs from that of the deficit in ouabain-sensitive ATPase.
在对照大鼠和链脲佐菌素诱导的病程为8周的糖尿病大鼠的坐骨神经匀浆中，测量哇巴因敏感的ATP酶活性（以每小时每毫克（湿）神经产生的nmol ADP表示±标准误）。糖尿病大鼠的神经显示出的活性（21.7±2.0）显著低于对照组（34.6±4.8）（p<0.05）。这些动物还表现出坐骨神经运动神经元传导速度（米/秒±标准误）的缺陷（对照组为57.7±0.7，糖尿病组为50.7±0.4；p<0.001）。同时，将匹配的对照组和糖尿病组大鼠每日腹腔注射从牛脑中提取的混合神经节苷脂（10mg/kg）。经过8周的这种治疗后，糖尿病组未出现哇巴因敏感的ATP酶活性缺陷（治疗后的糖尿病组为31.9±3.7，治疗后的对照组为34.5±3.8）。然而，该治疗并未影响运动神经传导速度的缺陷（治疗后的糖尿病组为50.9±1.1，治疗后的对照组为57.9±0.5；p<0.001）。两个糖尿病组中多元醇途径代谢产物——山梨醇和果糖——的积累以及神经肌醇的消耗相似。这些数据表明传导速度缺陷的病因与哇巴因敏感的ATP酶缺陷的病因不同。
