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- Title
Common promoter polymorphism in monocyte differentiation antigen CD14 is associated with serum triglyceride levels and body mass index in non-diabetic individuals.
- Authors
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.
- Abstract
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/m2; 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.
- Subjects
GENETIC polymorphisms; BODY mass index; MONOCYTES; ANTIGENS; DIABETES; PEOPLE with diabetes; ENDOCRINE diseases
- Publication
Diabetic Medicine, 2006, Vol 23, Issue 1, p72
- ISSN
0742-3071
- Publication type
Article
- DOI
10.1111/j.1464-5491.2005.01732.x