Results revealed significant differences in rs670 and rs2292318 allele frequencies between cases and controls (P<0.025). rs670 G allele carriers were more likely to develop dyslipidemia than A allele carriers (OR = 1.315, OR 95% CI: 1.067-2.620; P = 0.010). rs2292318 T allele carriers were more likely to develop dyslipidemia than A allele carriers (OR = 1.264, OR 95% CI: 1.037-1.541; P = 0.020).
ApoB rs512535 and ApoA1 rs670 major G allele homozygotes had increased MetS risk (OR 1.65 [CI 1.24, 2.20], P = 0.0006; OR 1.42 [CI 1.08, 1.87], P = 0.013), which may be, partly, explained by their increased abdominal obesity and impaired insulin sensitivity (P<0.05) but not dyslipidemia.
Furthermore, the association of <i>APOA1</i> rs5072 in this gene cluster with dyslipidemia differed between genders; thus, additional studies are needed to confirm this conclusion, and the mechanisms underlying these results warrant further exploration.
Most importantly, the variant rs632153 is involved in elevating TC, LDLC, TG and VLDLs and probably playing a crucial role in the manifestation of dyslipidemia.
These findings indicate that the polymorphisms in the APOA1 gene (rs670, rs5069, and rs2070665) are not associated with dyslipidemia in the Kazakh population assessed in this study.
These findings indicate that the polymorphisms in the APOA1 gene (rs670, rs5069, and rs2070665) are not associated with dyslipidemia in the Kazakh population assessed in this study.