Raccah D, Fabreguetts C, Azulay J P, Vague P
Diabetes Department, University Hospital Timone, Marseille, France.
Diabetes Care. 1996 Jun;19(6):564-8. doi: 10.2337/diacare.19.6.564.
To study the relationship among red blood cell Na(+)-K(+)-ATPase activity, metabolic control, and diabetic neuropathy.
Na(+)-K(+)-ATPase activity has been measured in the red cell membrane of 43 long-standing IDDM patients (duration of diabetes 17.5 +/- 2 years, mean +/- SE), with 20 of the patients presenting with peripheral neuropathy. There were 23 healthy subjects serving as the control group.
Na(+)-K(+)-ATPase activity was significantly lower in diabetic patients than in healthy subjects (236.5 +/- 7.5 vs. 294 +/- 10 nmol P1 . mg protein-1 . h-1, P < 0.05). Among diabetic patients, Na+/K(+)-ATPase activity was not dependent on the degree of diabetic control, nor was it correlated with either fasting blood glucose (r = 0.16, NS) or HbA1 (r = 0.01, NS). Na(+)-K(+)-ATPase activity was lower in patients with neuropathy than in those without it (212 +/- 8.5 vs. 261 +/- 6.6, P < 0.05). Furthermore, in a subgroup of 20 patients, a positive correlation was observed between erythrocyte Na(+)-K(+)-ATPase activity and nerve conduction velocity in the peroneal (r = 0.558, P < 0.02) and tibial nerve (r = 0.528, P < 0.05).
These results suggest that diabetes-induced Na(+)-K(+)-ATPase activity dysfunction could be implicated in the pathogenesis of human diabetic neuropathy and the electrophysiological abnormalities observed in these patients.
研究红细胞钠钾ATP酶活性、代谢控制与糖尿病神经病变之间的关系。
对43例长期患胰岛素依赖型糖尿病患者（糖尿病病程17.5±2年，均值±标准误）的红细胞膜钠钾ATP酶活性进行了测定，其中20例患者伴有周围神经病变。选取23名健康受试者作为对照组。
糖尿病患者的钠钾ATP酶活性显著低于健康受试者（236.5±7.5对294±10 nmol P1·mg蛋白-1·h-1，P<0.05）。在糖尿病患者中，钠钾ATP酶活性不依赖于糖尿病控制程度，与空腹血糖（r=0.16，无显著性差异）或糖化血红蛋白（r=0.01，无显著性差异）均无相关性。有神经病变的患者钠钾ATP酶活性低于无神经病变者（212±8.5对261±6.6，P<0.05）。此外，在20例患者的亚组中，观察到红细胞钠钾ATP酶活性与腓总神经（r=0.558，P<0.02）和胫神经（r=0.528，P<0.05）的神经传导速度呈正相关。
这些结果提示，糖尿病诱导的钠钾ATP酶活性功能障碍可能与人类糖尿病神经病变的发病机制以及这些患者中观察到的电生理异常有关。
