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Background

Diabetic patients are at high risk of atherosclerotic complications, and factors associated with this include hypercholesterolemia, hemorheologic disturbances in erythrocytes and oxidative stress. We, therefore, carried out a study in type 2 diabetic patients to determine the relationships of erythrocyte Na+-K+ ATPase activity, plasma cholesterol and oxidative stress in this population.

Methods

Erythrocyte Na+-K+ ATPase activity and its relationship between plasma cholesterol and thiobarbituric acid reactive substance (TBARS, a marker of oxidative stress) were studied in type 2 diabetic patients with (n = 26) or without angiopathy (n = 30). Na+-K+ ATPase activity was measured by a colorimetric enzymatic method. Plasma TBARS levels were determined spectrophotometrically. Diabetic patients were classified according to plasma cholesterol concentrations as normo- or hypercholesterolemic (plasma total cholesterol > 5.18 mmol/L).

Results

Diabetic patients with or without angiopathy had lower erythrocyte Na+-K+ ATPase activity (p < 0.001 and p < 0.001 respectively) and higher plasma TBARS levels than healthy subjects (n = 20) (p < 0.001 and p < 0.001 respectively). Na+-K+ ATPase activity in the diabetic patients with angiopathy was lower than in the diabetic patients without angiopathy (p < 0.001). In the diabetic patients both with and without angiopathy, hypercholesterolemic patients had lower erythrocyte Na+-K+ ATPase activity and higher plasma TBARS levels than normocholesterolemic patients (p < 0.001, p < 0.001 respectively) There was no difference in the plasma TBARS concentrations between diabetic patients with and without angiopathy. There were negative correlations between erythrocyte Na+-K+ ATPase activity and both plasma cholesterol (r = -0.72) and plasma TBARS (r = -0.46) and a positive correlation between plasma cholesterol and TBARS (r = 0.42).

Conclusions

Elevated plasma cholesterol may be responsible for the inhibition of erythrocyte Na+-K+ ATPase activity. Together with elevated cholesterol, free radical-induced mechanisms may be involved in the inhibition of Na+-K+ ATPase activity."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/author"Hatemi H."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/author"Kemerli G.D."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/author"Konukoglu D."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/author"Sabuncu T."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/name"Clin Invest Med"xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/pages"279-284"xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/title"Relation of erythrocyte Na+-K+ ATPase activity and cholesterol and oxidative stress in patients with type 2 diabetes mellitus."xsd:string
http://purl.uniprot.org/citations/14690302http://purl.uniprot.org/core/volume"26"xsd:string
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