BACKGROUND: Type 2 diabetes mellitus (T2DM) is a multifactorial disease resulting from ineffective use of insulin in the body. Single nucleotide polymorphisms (SNPs) in genes for scavenger receptors such as CD36 have been implicated in the pathogenesis of atherosclerosis and cardiovascular diseases in diabetes. The present study evaluated the effect of genetic polymorphisms of the CD36 gene on the risk of developing T2DM. Four SNPs in the CD36 gene (-178A→C in the promoter region, rs1984112 [A→G in exon 1A], rs1527479 [T→C in intron IB], and rs3211938 [T→G in exon 10]) were screened in T2DM patients and healthy controls (n=100 each). MATERIALS AND METHODS: Analysis of CD36 gene polymorphisms was performed by polymerase chain reaction-restriction fragment length polymorphism. Statistical analysis was done by Fisher's exact test and χ² statistics using SPSS version 15.0 software (SPSS, Inc., Chicago, IL), whereas SHEsis software (available at http://analysis.bio-x.cn/myAnalysis.php ) was used for haplotype analysis. RESULTS: There was genotypic association of rs3211938 (T→G) polymorphism with T2DM (P=0.046), whereas rs1984112 (A→G) and rs1527479 (T→C) SNPs showed no association. The minor alleles of SNPs ("G" of rs1984112, "C" of rs1527479, and "G" of rs3211938) showed significant association with clinical profiles in T2DM patients (P<0.05). Analysis also showed that the "GCG" haplotype had a significant association with T2DM (P=0.026; odds ratio=3.12; 95% confidence interval 1.089-8.939). Significant association of the CD36 gene was confirmed by linkage disequilibrium patterns. CONCLUSIONS: The CD36 variants may help to determine the T2DM susceptibility in the North Indian population. However, genotyping of variants in more individuals and studies in other populations will be required to validate the results and ethnic variations.
BACKGROUND:Type 2 diabetes mellitus (T2DM) is a multifactorial disease resulting from ineffective use of insulin in the body. Single nucleotide polymorphisms (SNPs) in genes for scavenger receptors such as CD36 have been implicated in the pathogenesis of atherosclerosis and cardiovascular diseases in diabetes. The present study evaluated the effect of genetic polymorphisms of the CD36 gene on the risk of developing T2DM. Four SNPs in the CD36 gene (-178A→C in the promoter region, rs1984112 [A→G in exon 1A], rs1527479 [T→C in intron IB], and rs3211938 [T→G in exon 10]) were screened in T2DM patients and healthy controls (n=100 each). MATERIALS AND METHODS: Analysis of CD36 gene polymorphisms was performed by polymerase chain reaction-restriction fragment length polymorphism. Statistical analysis was done by Fisher's exact test and χ² statistics using SPSS version 15.0 software (SPSS, Inc., Chicago, IL), whereas SHEsis software (available at http://analysis.bio-x.cn/myAnalysis.php ) was used for haplotype analysis. RESULTS: There was genotypic association of rs3211938 (T→G) polymorphism with T2DM (P=0.046), whereas rs1984112 (A→G) and rs1527479 (T→C) SNPs showed no association. The minor alleles of SNPs ("G" of rs1984112, "C" of rs1527479, and "G" of rs3211938) showed significant association with clinical profiles in T2DM patients (P<0.05). Analysis also showed that the "GCG" haplotype had a significant association with T2DM (P=0.026; odds ratio=3.12; 95% confidence interval 1.089-8.939). Significant association of the CD36 gene was confirmed by linkage disequilibrium patterns. CONCLUSIONS: The CD36 variants may help to determine the T2DM susceptibility in the North Indian population. However, genotyping of variants in more individuals and studies in other populations will be required to validate the results and ethnic variations.