Genetics & Epigenetics

Objective: Visfatin is a novel adipokine initially reported to exhibit insulin-mimetic effects that increase insulin sensitivity. Further studies indicate it may also be associated with obesity, serum lipids, and systemic inflammation. At the current time, the role of genetic variation in the visfatin gene (NAMPT) on these parameters is not clear. In the present study, we examined the association between 10 SNPs in NAMPT and insulin resistance, obesity, serum lipids and hsCRP levels.

Research design and methods: A total of 1838 subjects (413 men, 1425 women) were recruited from the ongoing CODING Study. All subjects were from the genetically homogenous population of Newfoundland and Labrador, Canada. BMI, waist circumference, waist-to-hip ratio, and body fat percentage (determined using DXA) were measured for all subjects. Serum glucose, insulin, HOMAIR, HOMAβ, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides and hsCRP were also determined after a 12-hour fast. Ten SNPs in NAMPT were genotyped using TaqMan validated or functionally tested SNP genotyping assays including rs7789066 (A . G 5’ flanking region), rs3801266 (A > G intron), rs6963243 (G > C intron), rs2058539 (A > C intron), rs6947766 (C > T intron), rs4730153 (G > A intron), rs10808150 (G > A intron), rs2098291 (C > T intron), rs10953502 (T > C intron), and rs10953501 (A > G 3’ UTR).

Results: We observed no significant associations between any of the variants sites and any parameter of insulin resistance, body composition, serum lipids or hsCRP under an additive model with age and gender included as covariates. This was also true when both dominant and recessive models were applied.

Conclusions: Our results do not support a significant role for variations in NAMPT with differences in the measured variables in the Newfoundland population.