BACKGROUNDS: Insulin resistance plays a major role in the pathogenesis of the metabolic syndrome. Inflammation is the leading cause of insulin resistance, and interleukin 10 (IL-10) is one of the anti-inflammatory cytokines. We conducted a case-control study to investigate the association between the IL-10 polymorphisms and the metabolic syndrome. METHODS: One thousand two hundred two unrelated subjects residing in southern Taiwan were retrospectively recruited from a community-based health screening program. Two hundred sixty subjects were defined as the metabolic syndrome (3-5 risk components) and 549 subjects as controls (0-1 risk component) on the basis of the Asian version of the Adult Treatment Panel III criteria. A functional IL-10 single nucleotide polymorphism (SNP; rs1800871) and 2 tagging SNPs (rs3790622, rs3021094) were genotyped by TaqMan method. RESULTS: We analyzed the association between the genotypes and the presence of the metabolic syndrome or metabolic traits by χ² test and multivariant logistic regression. None of the IL-10 SNPs were found to be significantly related with the metabolic syndrome or its risk components. All the 3 SNPs were in single linkage disequilibrium block. Haplotype analysis did not yield significant association between IL-10 gene and the metabolic syndrome (global P = 0.88). CONCLUSIONS: Because we used tagging SNPs and a modest clinical cohort, we concluded that the IL-10 gene polymorphisms may be unlikely to play an important role for the metabolic syndrome.
BACKGROUNDS: Insulin resistance plays a major role in the pathogenesis of the metabolic syndrome. Inflammation is the leading cause of insulin resistance, and interleukin 10 (IL-10) is one of the anti-inflammatory cytokines. We conducted a case-control study to investigate the association between the IL-10 polymorphisms and the metabolic syndrome. METHODS: One thousand two hundred two unrelated subjects residing in southern Taiwan were retrospectively recruited from a community-based health screening program. Two hundred sixty subjects were defined as the metabolic syndrome (3-5 risk components) and 549 subjects as controls (0-1 risk component) on the basis of the Asian version of the Adult Treatment Panel III criteria. A functional IL-10 single nucleotide polymorphism (SNP; rs1800871) and 2 tagging SNPs (rs3790622, rs3021094) were genotyped by TaqMan method. RESULTS: We analyzed the association between the genotypes and the presence of the metabolic syndrome or metabolic traits by χ² test and multivariant logistic regression. None of the IL-10 SNPs were found to be significantly related with the metabolic syndrome or its risk components. All the 3 SNPs were in single linkage disequilibrium block. Haplotype analysis did not yield significant association between IL-10 gene and the metabolic syndrome (global P = 0.88). CONCLUSIONS: Because we used tagging SNPs and a modest clinical cohort, we concluded that the IL-10 gene polymorphisms may be unlikely to play an important role for the metabolic syndrome.