ABSTRACT
Metabolic syndrome (MetS) is complex and determined by the interaction between genetic and environmental factors and their influence on obesity, insulin resistance, and related traits associated with diabetes and cardiovascular disease risk. Some dynamic markers, including adiponectin (ADIPOQ), brain-derived neurotrophic factor (BDNF), and lipoprotein lipase (LPL), are implicated in MetS; however, the influence of their genetic variants on MetS susceptibility varies in racial and ethnic groups. We investigated the association of single nucleotide polymorphism (SNP)-SNP interactions among nine SNPs in six genes with MetS's genetic predisposition in Mongolian subjects. A total of 160 patients with MetS for the case group and 144 healthy individuals for the control group were selected to participate in this study. Regression analysis of individual SNPs showed that the ADIPOQ + 45GG (odds ratio (OR) = 2.09, p = 0.011) and P+P+ of LPL PvuII (OR = 2.10, p = 0.038) carriers had an increased risk of MetS. Conversely, G allele of LPL S447X (OR = 0.45, p = 0.036) and PGC-1α 482Ser (OR = 0.26, p = 0.001) allele were estimated as protective factors, respectively. Moreover, a haplotype containing the G-P+-G combination was related to MetS. Significant loci were also related to body mass index (BMI), systolic blood pressure (SBP), serum high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and fasting blood glucose (FBG), adipokines, and insulin as well as insulin resistance (p < 0.05). Our results confirm that ADIPOQ + 45T > G, LPL PvII, and PGC-1α Gly482Ser loci are associated with MetS in Mongolian subjects.
ABSTRACT
Metabolic syndrome (MetS) corresponds with multiple risk factors. Many studies have indicated that MetS significantly increases the risk of cardiovascular diseases and type 2 diabetes (T2D). The prevalence of MetS was estimated to be one third of the general Mongolian population in 2015. The purpose of our study was to determine polymorphisms of the LEP (Leptin) and LEPR (Leptin receptor) genes that show susceptibility to MetS and to predict the genetic risk of MetS. We selected 160 cases with MetS and 144 with healthy controls. The G2548A polymorphism of the LEP gene and the A668G (Q223R) polymorphism of the LEPR gene were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The results of the regression analysis showed that the 2548 amino acids (AA) of LEP gene carriers had increased incidences of MetS (OR = 3.23; p = 0.035), and the combined genotype AA/AA of LEP and LEPR gene polymorphisms was related to the development of MetS (OR = 3.73; p = 0.047). Patients with MetS who were 2548A allele carriers had an increased concentration of serum leptin (p = 0.011). Moreover, G2548A of LEP polymorphism was associated with elevated body mass index (BMI) and fasting blood glucose (FBG) in the case group. Our results confirm that the LEP G2548A loci is the independent risk factor of MetS.
