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Common promoter polymorphism in monocyte differentiation antigen CD14 is associated with serum triglyceride levels and body mass index in non‐diabetic individuals
Author(s) -
Shin H. D.,
Park K. S.,
Park B. L.,
Cheong H. S.,
Cho Y. M.,
Lee H. K.,
Lee J.Y.,
Lee J.K.,
Kim H. T.,
Han B. G.,
Kim J. W.,
Koh I.,
Kim Y. J.,
Oh B.,
Kimm K.,
Park C.
Publication year - 2006
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2005.01732.x
Subject(s) - cd14 , medicine , endocrinology , body mass index , minor allele frequency , immunology , single nucleotide polymorphism , allele , genotype , genetics , biology , gene , receptor
Aims Growing evidence supports the hypothesis that chronic low‐grade inflammation related to innate immunity may play an important role in the pathophysiology of Type 2 diabetes mellitus (T2DM). The monocyte differentiation antigen CD14 gene ( CD14 ) acts as the receptor for lipopolysaccharide (LPS) and augments monocyte/macrophage inflammatory responses. Methods We have sequenced the gene, including all exons, exon/intron boundaries, and the −1.5 kb of the 5′ flanking region. Two common loci (minor allele frequency > 0.05) were genotyped in 775 T2DM patients and 316 control subjects recruited in the Korean T2DM Study. Results Eight polymorphisms, including four non‐synonymous forms, were identified in CD14 . No polymorphisms were found in association with T2DM. However, one common promoter SNP ( −260T>C ) was significantly associated with both the serum triglyceride level (TG) and body mass index (BMI) in non‐diabetic control subjects. Individuals who carried the minor allele (C) had higher TG levels (1.65 ± 0.81 vs. 1.46 ± 0.80 mmol/l; P = 0.0007) and BMI (23.96 ± 3.00 vs. 23.28 ± 3.22 kg/m 2 ; P = 0.04) as compared with subjects carrying T/T genotypes. Conclusion Our data suggest that lipid metabolism and obesity, important pathophysiological elements of T2DM and the metabolic syndrome, are regulated by complex mechanisms that include the CD14 gene polymorphism‐mediated genetic propensity to non‐specific inflammatory responses.