Our findings warrant further investigation of the mechanism of LPL on the development of obesity along with the role of intron one and its impact on LPL gene activity. Our study shows intron one polymorphism rs1534649 to increase the risk of obesity and dyslipidemia.
However, a trend was observed between the A-allele and increased BMI β = 1.75 (95% CI 0.14 – 3.35) p=0.03.
There were no associations between rs28645722 and plasma lipid levels (p>0.05). In addition, a borderline significance was observed between the T-allele and low levels of high density lipoprotein-cholesterol β = -0.04 (95% CI -0.08, -0.006) p=0.02. Using an additive genetic model, linear regression analysis showed the T-allele of rs1534649 to be associated with increased BMI in a dose-dependent trend β = 2.13 (95% CI 1.33 – 2.94) p=1.7x10⁻⁷. The relationship between the genotypes with both plasma lipid levels and BMI were assessed using linear regression using “SNPassoc” package from R statistical software. DNA samples were genotyped for two LPL gene polymorphisms (rs1534649 and rs28645722) using TaqMan allelic discrimination. We examined a total of 486 adults (303 and 183 females and males respectively) with plasma lipid levels and BMI. This study examined the association between LPL gene polymorphisms with plasma lipid levels and body mass index (BMI) in the Kuwaiti population. Single nucleotide polymorphisms (SNPs) across the LPL gene have been associated with dyslipidemia, however, the association with obesity has been limited towards specific populations. Lipoprotein lipase (LPL) is an enzyme involved in lipid metabolism and distribution of fatty acids hence its role in the initiation and development of dyslipidemia and adiposity.
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