Association between two common polymorphisms (single nucleotide polymorphism -250G/A and -514C/T) of the hepatic lipase gene and coronary artery disease in type 2 diabetic patients

Abstract

Background:Variations in the hepatic lipase (HL) gene are the potential candidate for coronary artery disease (CAD) especially in type 2 diabetes mellitus (T2DM) in diverse populations. We assessed the association of -514C/T and -250G/A polymorphisms in HL (LIPC) gene with CAD risk in Iranian population with type 2 diabetes.Materials and Methods:We evaluated 322 type 2 diabetic patients, 166 patients with normal angiograms as controls and 156 patients those identified with CAD undergoing their first coronary angiography as CAD cases. Genotyping of -514C/T and -250G/A polymorphisms in the promoter of the LIPC gene were studied by polymerase chain reaction (PCR)-restriction fragment length polymorphism technique.Results:Genotype distributions in CAD cases (73.7%, 20.5%, and 5.8% for −250G/A) and (62.2%, 32.7%, and 5.1% for -514C/T) were significantly different from those in controls (60.8%, 37.4%, and 1.8% for -250G/A) and (51.2%, 48.2%, and 0.6% for -514C/T). CAD cases had lower A-allele frequency than controls (0.131 vs. 0.196, P = 0.028). The odds ratio for the presence of -250 (GG + GA) genotype and A allele in CAD cases were 2.206 (95% confidence interval [CI] =1.33–3.65, P = 0.002) and 1.609 (95% CI = 1.051 −2.463, P = 0.029) respectively. Haplotype analysis demonstrated a significant association between especially LIPC double mutant (−250 A/-514 T) haplotype and presence of CAD.Conclusion:Our findings indicated that -250 G/A polymorphism rather than -514 C/T polymorphism of LIPC gene is more associated with the increased risk of CAD particularly in women with T2DM.

Effect of polymorphisms in interleukin-18 gene on the susceptibility to coronary artery disease in a Chinese population

“…CAD develops as a result of vascular tract stenosis or occlusion caused by coronary atherosclerotic lesions and several environmental and lifestyle factors (Campbell et al, 1998;Erbel and Görge, 2014;Bullock-Palmer, 2015). Previous experimental studies at the molecular level have indicated that many genetic factors, including the genes encoding angiotensinogen and angiotensin-converting enzyme, hepatic lipase, insulin receptor substrate-1, kinesin family member 6, cholesteryl ester transfer protein, ATP-binding cassette subfamily A member 1, and apoptotic extrinsic death receptor, have an important role in the risk of CAD development (Bonfim-Silva et al, 2016;Cyrus et al, 2016;Kishore Kumar et al, 2016;Mohammadzadeh et al, 2016;Vatte et al, 2016;Zhang et al, 2016).…”

Contribution of adiponectin polymorphisms to the risk of coronary artery disease in a North‐African Tunisian population

“…Hou et al demonstrate that subgroup analyses based on ethnic group illuminated that +45T>G polymorphism is significantly associated with CAD risk among Arabians, with an overall ORs (95% CIs) of 1.65 (1.12‐2.42) for allelic frequency. However, in the same meta analysis, only three populations showed no association with CAD from the eight studied Arab populations including 2306 Arabians …”

“…First, Esteghamati et al on a study of 114 type 2 diabetic subjects with CAD, and 127 type 2 diabetic patients without CAD revealed that two haplotypes 45T‐276T and 45G‐276T were associated with a decreased risk of CAD [adjusted OR = 0.47 (95% CI: 0.32–0.94); P = .03 and adjusted OR = 0.33 (95% CI: 0.13–0.83); P = .02, respectively]. Second, Mohammadzadeh et al found that the haplotype consisting of mutant allele of SNP +45 and wild allele of SNP +276 was more prevalent in CAD cases compared to the controls (OR = 0.37, 95% CI = 0.16‐0.86, P = .022).…”

Association study of the single‐nucleotide polymorphisms −3971G/A and +276G/T in the adiponectin gene with type 2 diabetes in a North Indian Punjabi population

“…The genotyping of ADIPOQ polymorphisms (−3971A/G and +276G/T) was performed using polymerase chain reaction–based restriction fragment length polymorphism (PCR‐RFLP) methods. The primers and restriction enzymes used were taken from previously reported studies and are listed in Table (Mohammadzadeh, Ghaffari, Heibar, & Bazyar, ; Ramya et al., ).…”