Diabetes Care, Vol 19, Issue 6 564-568, Copyright © 1996 by American Diabetes Association

ARTICLES

Erythrocyte Na(+)-K(+)-ATPase activity, metabolic control, and neuropathy in IDDM patients

D Raccah, C Fabreguetts, JP Azulay and P Vague
Diabetes Department, University Hospital Timone, Marseille, France.

OBJECTIVE: To study the relationship among red blood cell Na(+)-K(+)-ATPase activity, metabolic control, and diabetic neuropathy. RESEARCH DESIGN AND METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.
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