ERYTHROCYTE NA-K+-ATPASE ACTIVITY, METABOLIC CONTROL, AND NEUROPATHY IN IDDM PATIENTS()

Citation
D. Raccah et al., ERYTHROCYTE NA-K+-ATPASE ACTIVITY, METABOLIC CONTROL, AND NEUROPATHY IN IDDM PATIENTS(), Diabetes care, 19(6), 1996, pp. 564-568
Citations number
28
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
01495992
Volume
19
Issue
6
Year of publication
1996
Pages
564 - 568
Database
ISI
SICI code
0149-5992(1996)19:6<564:ENAMCA>2.0.ZU;2-A
Abstract
OBJECTIVE- To study the relationship among red blood cell Na+-K+-ATPas e activity, metabolic control, and diabetic neuropathy. RESEARCH DESIG N AND METHODS- Na+-K+-ATPase activity has been measured in the red cel l membrane of 43 long-standing IDDM patients (duration of diabetes 17. 5 +/- 2 years, mean +/- SE), with 20 of the patients presenting with p eripheral neuropathy. There were 23 healthy subjects serving as the co ntrol group. RESULTS- Na+-K+-ATPase activity was significantly lower i n diabetic patients than in healthy subjects (236.5 +/- 7.5 vs. 294 +/ - 10 nmol P, . mg protein(-1) . h(-1), P < 0.05). Among diabetic patie nts, Na+/K+-ATPase activity was not dependent on the degree of diabeti c control, nor was it correlated with either fasting blood glucose (r = 0.16, NS) or HbA(1c) (r = 0.01, NS). NA(+)-K+-ATPase activity was lo wer 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 erthrocyte 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 resu lts suggest that diabetes-induced Na+-K+-ATPase activity dysfunction c ould be implicated in the pathogenesis of human diabetic neuropathy an d the electrophysiological abnormalities observed in these patients.