BMC Endocrine Disorders
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Research articleAssociation between erythrocyte Na+K+-ATPase activity and some blood lipids in type 1 diabetic patients from Lagos, NigeriaBamidele A Iwalokun1 and Senapon O Iwalokun2  1
Dept of Biochemistry, Lagos State University, PMB. 1087, Apapa-Lagos, Nigeria 2
Dept. of Endocrinology, Faculty of Clinical Science, Lagos State University, College of Medicine, Ikeja – Lagos, PMB. 21266, Ikeja – Lagos, Nigeria author email corresponding author email
BMC Endocrine Disorders 2007,
7:7doi:10.1186/1472-6823-7-7
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| Published: |
1 October 2007 |
Abstract
Background
Altered levels of erythrocyte Na+K+-ATPase, atherogenic and anti-atherogenic lipid metabolites have been implicated in diabetic complications but their pattern of interactions remains poorly understood.
This study evaluated this relationship in Nigerian patients with Type 1 diabetes mellitus.
Methods
A total of 34 consented Type 1 diabetic patients and age -matched 27 non-diabetic controls were enrolled. Fasting plasma levels of total cholesterol, triglycerides and HDL-cholesterol were determined spectrophotometrically and LDL-cholesterol estimated using Friedewald formula. Total protein content and Na+K+-ATPase activity were also determined spectrophotometrically from ghost erythrocyte membrane prepared by osmotic lysis.
Results
Results indicate significant (P < 0.05) reduction in Na+K+-ATPase activity in the Type 1 diabetic patients (0.38 ± 0.08 vs. 0.59 ± 0.07 uM Pi/mgprotein/h) compared to the control but with greater reduction in the diabetic subgroup with poor glycemic control (n = 20) and in whom cases of hypercholesterolemia (8.8%), hypertriglyceridemia (2.9%) and elevated LDL-cholesterol (5.9% each) were found. Correlation analyses further revealed significant (P < 0.05) inverse correlations [r = -(0.708-0.797] between all the atherogenic lipid metabolites measured and Na+K+-ATPase in this subgroup contrary to group with good glycemic control or non-diabetic subjects in which significant (P < 0.05) Na+K+-ATPase and HDL-C association were found (r = 0.427 - 0.489). The Na+K+-ATPase from the diabetic patients also exhibited increased sensitivity to digoxin and alterations in kinetic constants Vmax and Km determined by glycemic status of the patients.
Conclusion
It can be concluded that poor glycemic control evokes greater reduction in erythrocyte Na+K+-ATPase activity and promote enzyme-blood atherogenic lipid relationships in Type 1 diabetic Nigerian patients. |