Diabetes research and clinical practice · 2008
HbA1c negatively correlates with LCAT activity in type 2 diabetes.
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Nakhjavani Manouchehr, Esteghamati Alireza, Esfahanian Fatemeh, Ghanei Azam, Rashidi Armin, Hashemi Saeideh
Аннотация
AIMS: Abnormal high-density lipoproteins (HDL) metabolism is a major cardiovascular risk factor in type 2 diabetes mellitus (DM2). Lecithin:cholesterol acyltransferase (LCAT) increases HDL size by transferring 2-acyl groups from lecithin or phosphatidylethanolamine to unesterified cholesterol. The purpose of this study was to determine the independent correlates of LCAT activity in DM2 patients.
METHODS: A total of 45 (male: 20) consecutive adult DM2 patients aging 50.0+/-7.0 years (range: 40-64 years) with a median diabetes duration of 4 years (range: 2-18) were studied. Exclusion criteria were: smoking, positive history of cardiovascular, thyroid, renal or liver disease, pregnancy, treatment with metformin, insulin, lipid lowering drugs, angiotensin-converting enzyme inhibitors, aspirin or antioxidant supplements. Univariate and multivariate analyses were performed.
RESULTS: From a comprehensive list of variables studied, only HbA1c (rho=-0.951) and oxidized LDL (rho=-0.779) had statistically significant correlation with LCAT activity (p<0.001). These two variables were themselves strongly correlated to each other (rho=0.809, p<0.001). To eliminate potential confounding effects, we performed multivariate analysis, where HbA1c emerged as a strong independent predictor of LCAT activity (adjusted OR=-0.928, p<0.001).
CONCLUSIONS: Glycemia-induced glycation of HDL decreases LCAT activity. The fact that HbA1c is an accurate measure of glycation and can therefore reflect glycated HDL levels explains the association found in the present study. In conclusion, HbA1c provides an easy-to-assess, accurate measure of LCAT activity in DM2.
METHODS: A total of 45 (male: 20) consecutive adult DM2 patients aging 50.0+/-7.0 years (range: 40-64 years) with a median diabetes duration of 4 years (range: 2-18) were studied. Exclusion criteria were: smoking, positive history of cardiovascular, thyroid, renal or liver disease, pregnancy, treatment with metformin, insulin, lipid lowering drugs, angiotensin-converting enzyme inhibitors, aspirin or antioxidant supplements. Univariate and multivariate analyses were performed.
RESULTS: From a comprehensive list of variables studied, only HbA1c (rho=-0.951) and oxidized LDL (rho=-0.779) had statistically significant correlation with LCAT activity (p<0.001). These two variables were themselves strongly correlated to each other (rho=0.809, p<0.001). To eliminate potential confounding effects, we performed multivariate analysis, where HbA1c emerged as a strong independent predictor of LCAT activity (adjusted OR=-0.928, p<0.001).
CONCLUSIONS: Glycemia-induced glycation of HDL decreases LCAT activity. The fact that HbA1c is an accurate measure of glycation and can therefore reflect glycated HDL levels explains the association found in the present study. In conclusion, HbA1c provides an easy-to-assess, accurate measure of LCAT activity in DM2.