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Erythrocyte Na+-K+-ATPase Activity, Metabolic Control, and Neuropathy in IDDM Patients

  1. Denis Raccah, MD, PHD,
  2. Claudie Fabreguettes, MD,
  3. Jean-Philippe Azulay, MD and
  4. Phillippe Vague, MD, PHD
  1. Diabetes Department, University Hospital Timone Marseille, France
  1. Address correspondence and reprint requests to Denis Raccah, MD, PhD, Hopital Timone, Boulevard Jean Moulin, 13385 Marseille Cedex 5, France

Abstract

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 HbA1c (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.

  • Received September 20, 1995.
  • Revision received January 11, 1996.
  • Accepted January 11, 1996.
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