Abstract
BackgroundEvidence of the genetic association between CD36 candidate gene and the risk of metabolic syndrome and its components has been inconsistent. This case–control study assessed the haplotype-tagged SNPs from CD36 on the risk of metabolic syndrome and components.Methods and resultsWe recruited 1,000 cases and age, gender-matched controls were randomly selected from the participants with metabolic syndrome defined by International Diabetes Federation. Overall, the haplotype tagged SNPs of CD36 gene were not related to the risk of metabolic syndrome. For individuals with normal lipid levels, several SNPs were significantly associated with the triglycerides and HDL-cholesterol levels: Subjects with rs3211848 homozygote had a higher triglyceride level (99.16 ± 2.61 mg/dL), compared with non-carriers (89.27 ± 1.45 mg/dL, P = 0.001). In addition, compared with non-carriers, individuals with rs1054516 heterozygous and homozygous genotypes had a significantly lower HDL-cholesterol (46.6 ± 0.46 mg/dL for non-carrier, 44.6 ± 0.36 mg/dL for heterozygous, and 44.3 ± 0.56 mg/dL for homozygous, P = 0.0008).ConclusionThe CD36 gene variants were significantly associated with triglycerides and HDL-cholesterol concentrations among ethnic Chinese in Taiwan.
Highlights
The CD36 is a glycoprotein located in membrane and plays various cellular processes such as lipid transport, immune regulation, coagulation and atherosclerosis [1], and the CD36 structure is related to scavenger receptor B1, and highly binds to oxidized LDL [2], which induced atherosclerosis process
The CD36 gene variants were significantly associated with triglycerides and HDL-cholesterol concentrations among ethnic Chinese in Taiwan
From the pilot genotyping results, we found that several CD36 gene SNPs were associated with metabolic syndrome status and metabolic trait, including HDL, triglycerides, body mass index, fasting glucose and triglyceride levels (Additional file 1: Table S2)
Summary
The CD36 is a glycoprotein located in membrane and plays various cellular processes such as lipid transport, immune regulation, coagulation and atherosclerosis [1], and the CD36 structure is related to scavenger receptor B1, and highly binds to oxidized LDL [2], which induced atherosclerosis process. CD36 gene variants regulated fatty acid metabolism and accumulation of fat and fat metabolites, and may influence the risk of metabolic syndrome and may be a target for further personalized medicine screening [3]. Emerging evidence indicating that variation in the CD36 gene may play a role in the pathogenesis of and components using a case–control study among ethnic Chinese adults, controlling for clinical and lifestyle factors. Evidence of the genetic association between CD36 candidate gene and the risk of metabolic syndrome and its components has been inconsistent. This case–control study assessed the haplotype-tagged SNPs from CD36 on the risk of metabolic syndrome and components
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