De La Tour D D, Raccah D, Jannot M F, Coste T, Rougerie C, Vague P
Department of Diabetes, University Hospital Timone, Marseille, France.
Diabetologia. 1998 Sep;41(9):1080-4. doi: 10.1007/s001250051033.
Erythrocyte Na/K ATPase activity is decreased in Type I diabetic patients; for Type II diabetic patients, literature data are controversial. Therefore, we have compared this enzymatic activity in 81 patients with Type I diabetes mellitus, 87 with Type II diabetes mellitus and 75 control subjects. Mean erythrocyte Na/K ATPase activity was lower in the Type I diabetic patients (285 +/- 8 nmol Pi x mg protein(-1) x h(-1)) than in the control subjects (395 +/- 9 nmol Pi x mg protein(-1) x h(-1)) whereas that of the Type II diabetic patients did not differ from that of control subjects. Sex, age, body mass index, and HbA1c levels did not influence erythrocyte Na/K ATPase activity. The 25 Type II diabetic patients treated with insulin, however, had lower Na/K ATPase activity than the 62 on oral treatment (264 +/- 18 vs 364 +/- 16 nmol Pi x mg protein(-1) x h(-1), p < 0.001) but similar to that of Type I diabetic patients. Among the Type II diabetic patients, stepwise regression analysis showed that fasting C-peptide level was the only factor independently correlated with Na/K ATPase activity; it explained 23% of its variance. In fact, in the insulin-treated patients, those with almost total endogenous insulin deficiency (C-peptide < 0.2 nmol x l(-1)) had the lower Na/K ATPase activity (181 +/- 21 vs 334 +/- 17 nmol Pi x mg protein(-1) x h(-1), p < 0.0001). The biological effects of treatment with C-peptide have recently led to the suggestion that this peptide could have a physiological role through the same signalling pathway as insulin, involving G-protein and calcium phosphatase and thus restoring Na/K ATPase activity. The relationship we describe between endogenous C-peptide and this activity is a strong argument for this physiological role.
I型糖尿病患者的红细胞钠钾ATP酶活性降低；对于II型糖尿病患者，文献数据存在争议。因此，我们比较了81例I型糖尿病患者、87例II型糖尿病患者和75例对照者的这种酶活性。I型糖尿病患者的平均红细胞钠钾ATP酶活性（285±8 nmol Pi×mg蛋白质⁻¹×h⁻¹）低于对照者（395±9 nmol Pi×mg蛋白质⁻¹×h⁻¹），而II型糖尿病患者的该活性与对照者无差异。性别、年龄、体重指数和糖化血红蛋白水平均不影响红细胞钠钾ATP酶活性。然而，25例接受胰岛素治疗的II型糖尿病患者的钠钾ATP酶活性低于62例接受口服治疗的患者（264±18 vs 364±16 nmol Pi×mg蛋白质⁻¹×h⁻¹，p<0.001），但与I型糖尿病患者相似。在II型糖尿病患者中，逐步回归分析显示空腹C肽水平是唯一与钠钾ATP酶活性独立相关的因素；它解释了其23%的变异。事实上，在接受胰岛素治疗的患者中，那些几乎完全缺乏内源性胰岛素（C肽<0.2 nmol×l⁻¹）的患者钠钾ATP酶活性较低（181±21 vs 334±17 nmol Pi×mg蛋白质⁻¹×h⁻¹，p<0.0001）。最近，C肽治疗的生物学效应提示该肽可能通过与胰岛素相同的信号通路发挥生理作用，涉及G蛋白和钙磷酸酶，从而恢复钠钾ATP酶活性。我们所描述的内源性C肽与该活性之间的关系有力地支持了这一生理作用。
