Study on Association of APOB Gene Polymorphism with Glycation of Low Density Lipoproteinin Type 2 DiabetesKapil Dev1, Seema Garg1, Suman B Sharma1*, Amitesh Aggarwal2and Madhu SV2
- *Corresponding Author:
- Dr. S B Sharma
Professor, Department of Biochemistry
University College of Medical
Sciences (University of Delhi) and G.T.B. Hospital
Dilshad Garden, Delhi-110095, India
Tel: +91 9818041119
E-mail: [email protected]
Received date: April 15, 2015; Accepted date: May 14, 2015; Published date: May 20, 2015
Citation: Dev K, Garg S, Sharma SB, Aggarwal A, Madhu SV (2015) Study on Association of APOB Gene Polymorphism with Glycation of Low Density Lipoproteinin Type 2 Diabetes. J Diabetes Metab 6:553. doi: 10.4172/2155-6156.1000553
Copyright: © 2015 Dev K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objectives: Sustained hyperglycemia results in non-enzymatic glycation of Apo B or LDL particle which may affect its recognition and uptake. Increase in circulating LDL levels is a vital contributor for atherosclerosis. APOB gene (c.12669 G>A, p.GLN4154LYS) polymorphism is believed to be associated with coronary artery disease. We thus designed our study to evaluate association of APOB gene polymorphism with Apo B glycation in type 2 diabetic patients. Methods: A total of 45 non diabetic controls and 45 type 2 diabetic patients participated in this study. Following an overnight fast, venous blood was collected and analyzed for glycemic status, lipid profile and other biochemical parameters. Apo B was estimated using nephelometry, Glycated LDL was estimated by ELISA. PCR-RFLP was used to determine the DNA polymorphism in the APOB gene using EcoR1. Results: Polymorphic analysis of APOB gene in diabetic population showed 73.3% wild type (R+/R+), 20.0% heterozygous mutant (R+/R-) and 6.7% homozygous mutant (R-/R-). Significant associations of glycated LDL was observed with R-/R- and R+/ R- when compared with R+/R+. Significant association was not observed between Apo B levels and of genotypes. Conclusions: Presence of polymorphism may not affect the expression Apo B level but acts as an important contributor to LDL modification and increases its glycation. Since glycation of LDL reduces uptake of LDL by LDL receptors, it may increase the risk of atherosclerosis.