title: Erythrocyte Na/K ATPase activity and diabetes: relationship with C-peptide level.
abstract: 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.
authors.affiliation: Department of Diabetes, University Hospital Timone, Marseille, France.
authors.forename: D D
authors.initials: DD
authors.lastname: De La Tour
authors.forename: D
authors.initials: D
authors.lastname: Raccah
authors.forename: M F
authors.initials: MF
authors.lastname: Jannot
authors.forename: T
authors.initials: T
authors.lastname: Coste
authors.forename: C
authors.initials: C
authors.lastname: Rougerie
authors.forename: P
authors.initials: P
authors.lastname: Vague
mesh_terms: D000328:Adult; D000368:Aged; D002096:C-Peptide / Q000097:blood*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000201:enzymology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000201:enzymology*; D004912:Erythrocytes / Q000201:enzymology*; D005215:Fasting; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood*
chemical_list: D002096:C-Peptide; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D000254:Sodium-Potassium-Exchanging ATPase