ERYTHROCYTE NA K ATPASE ACTIVITY AND DIABETES - RELATIONSHIP WITH C-PEPTIDE LEVEL/

Erythrocyte Na/K ATPase activity is decreased in Type I diabetic patie nts; for Type II diabetic patients, literature data are controversial. Therefore, we have compared this enzymatic activity in 81 patients wi th Type I diabetes mellitus, 87 with Type II diabetes mellitus and 75 control subjects. Mean erythrocyte Na/K ATPase activity was lower in t he Type I diabetic patients (285 +/- 8 nmol Pi mg protein(-1) . h(-1)) than in the control subjects (395 +/- 9 nmol Pi . mg protein(-1) . h( -1)) whereas that of the Type II diabetic patients did not differ from that of control subjects. Sex, age, body mass index, and HbA(1c) leve ls 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 . mg protein(-1) . h(-1), p < 0.001) but similar to that of Type I diabetic patients. Among the Type II diabetic patients, stepwise regr ession analysis showed that fasting C-peptide level was the only facto r independently correlated with Na/K ATPase activity; it explained 23 % of its variance. In fact, in the insulin-treated patients, those wit h almost total endogenous insulin deficiency (C-peptide < 0.2 nmol . l (-1)) had the lower Na/K ATPase activity (181 +/- 21 vs 334 +/- 17 nmo l Pi . mg protein(-1) . 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 p athway as insulin, involving G-protein and calcium phosphatase and thu s restoring Na/K ATPase activity. The relationship we describe between endogenous C-peptide and this activity is a strong argument for this physiological role.