| BackgroundThe metabolic syndrome (MS) is a set of multiple cardiovascular risk factors in individuals gathered syndrome including obesity, dyslipidemia, insulin resistance, high blood pressure, whose main clinical consequences was cardiovascular damage. With the development of socio-economic and lifestyle changes, children and adolescents with metabolic syndrome prevalence was increasing year by year. Due to the various MS diagnostic criteria for children as well as the differences between the races, the incidence of metabolic syndrome worldwide vary approximately between3%-19%. Now that the metabolic syndrome is mainly influenced by some environmental factors such as socio-economic factors, dietary patterns, eating habits, physical activity and multiple predisposing gene loci. Physical activity is the most important environmental impact factor of the metabolic syndrome, studies have shown that there are obviously a significant dose-effect relationship between the rate of childhood obesity and physical activity, and exercise therapy can reduce the severity of the metabolic syndrome and the development process. PPARy gene participate in adipocyte differentiation, promoting preadipocyte the peroxidase enzyme proliferator activated receptor the proliferate and differentiate into mature fat cells, metabolic pathways involved in fat synthesis, promoting the storage of triglycerides in the fat cells in thecontrol fat storage and release of the body to maintain energy balance and promote adipocyte gene expression has a positive regulatory role, and therefore is closely between PPARy gene polymorphisms and metabolic syndrome. Adiponectin (adiponectin, APN) is an adipocytokines secreted by mature fat cells which closely associated with obesity, insulin resistance (IR) diabetes mellitus (T2DM) and other diseases. Whole genome the broadband scan showed susceptibility loci encoding of T2DM and metabolic syndrome human exist in adiponectin gene(ADIPOQ) area. In recent years, studies had found that PPARy gene Pro12Ala (rs1801282), C1431T (rs3856806), and ADIPOQ-11377C>G (rs266729) polymorphisms with the metabolic syndrome components closely related. To this end, the purpose of this study is to investigate the Pro12Ala, the C1431T and-11377C>G polymorphism and physical activity relationship with metabolic syndrome among children in Guangzhou City, as well as the interaction between physical activity and gene polymorphism for metabolic syndrome to provide new clues for genetic predisposition.MethodsInformation and samples of this study were derived from a children metabolic syndrome survey done by Dr. Liu Weijia among April to June in2009in Guangzhou. The study cases were those children were diagnosed as MS by De Ferranti standard. Those did not suffer from MS and with normal body mass index, waist-to-hip ratio, blood pressure, blood sugar, cholesterol and other metabolic indicators were randomly selected as controls. Children with heart, liver, endocrine, genetic, metabolic, kidney disease or regulate blood pressure, blood lipids children of drug use were not selected. Demographic characteristics, growth conditions, parents’ education level, family income, and physical activity of objects were collected. Pro12Ala (rs1801282), C1431T (rs3856806) and-11377C>G (rs266729) loci were genotyped using sequencing identification.The differences in demographic characteristics between the cases and controls were tested using the t test (for continuous variables) or χ2test (for categorical variables); Multivariate logistic regression models were used to assess the effects of physical activity and genotype on metabolic syndrome, controlling for the demographic characteristics such as gender, age, education level of father, mother’s education level, family income and development state. The interaction between physical activity and genotypes on metabolic syndrome were evaluated by multiplicative models.Results1. Children with CG/GG genotype of-11377C>G had increased metabolic syndrome risk compared to those with CC genotype [OR (95%):1.76(1.01-3.09)]. Pro12Ala and C143IT were not significantly associated with metabolic syndrome.2. Children with sufficient physical activity had a decreased metabolic syndrome compared to those with insufficient physical activity OR (95%):0.14(0.04-0.50)].3. There was an interaction between C1431T and-11377C>G genotype. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased metabolic syndrome risk [OR (95%CI):3.81(1.55-9.40)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with metabolic syndrome risk. The genotype of C1431T (CC/TT)/-11377C>G (CG/GG) had a increased metabolic syndrome risk compared to those with CC/CC [OR (95%CI)2.37(1.00-5.62)], which was smaller than the single effect of-11377C>G genotype.4. There was an interaction between-11377C>G genotype and physical activity. The-11377C>G (CG/GG)/insufficient physical activity had a increased metabolic syndrome risk[OR (95%CI:1.96(1.06-3.59)], and-11377C>G (CC)/sufficient physical activity had a decreased metabolic syndrome risk both compared to-11377C>G (CC)/insufficient physical activity.-11377C>G (CG/GG)/insufficient physical activity were not significantly associated with metabolic syndrome.5. Children with CG/GG genotype of-11377C>G had increased hypertension risk compared to those with CC genotype [OR (95%):1.92(1.02-3.60)].6. Children with CG/GG genotype of-11377C>G had increased overweight/obesity risk compared to those with CC genotype [OR (95%):2.20(95%CI, 1.13-4.27)].7. Pro12Ala and C1431T were not significantly associated with the components of metabolic syndrome.8. Children with sufficient physical activity had a decreased high blood pressure, high waist circumference, hypertriglyceride, overweight/obesity and low HDL risk, compared to those with insufficient physical activity [OR (95%CI):0.05(0.01-0.44)]5[(95%):0.15(0.04-0.55)],[(95%):0.10(0.02-0.47)],[(95%):0.18(0.05-0.67)],[(95%):0.06(0.01-0.51)].9. There was an interaction between C143IT and-11377C>G genotype to high blood pressure. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased high blood pressure risk [OR (95%CI):5.42(1.83-16.05)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with high blood pressure risk. Compared to those with C1431T (CC)/-11377C>G (CC), the genotype of C1431T (CC)/-11377C>G (CG/GG) had a increased high blood pressure risk [OR (95%CI):3.86(1.53-9.73)],[OR (95%CI):3.86(1.53-9.73)]. The genotype of C1431T (CT/TT)/-11377C>G (CG/GG) were not significantly associated with the components of high blood pressure.10. There was an interaction between C1431T and-11377C>G genotype to high waist circumference. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased high waist circumference risk [OR (95%CI):4.69(1.73-12.72)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with high waist circumference risk. Compared to those with C1431T (CC)/-11377C>G (CC), the genotype of C1431T (CC)/-11377C>G (CG/GG),(CT/TT)/CC and (CC)/(CG/GG) had a increased high waist circumference risk [OR (95%CI):3.83(1.65-8.88)],[OR (95%CI):2.78(1.31-5.90)],and [OR (95%CI):2.95(1.21-7.21)]. The joint action of C1431T/-11377C>G was smaller than the single effect of-11377C>G genotype.11. There was an interaction between C1431T and-11377C>G genotype to overweight/obesity. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased overweight/obesity risk [OR (95%CI):3.70(1.48-9.22)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with overweight/obesity risk. Compared to those with C1431T (CC)/-11377C>G(CC), the genotype of C1431T (CC)/-11377C>G (CG/GG),(CT/TT)/CC and (CC)/(CG/GG) had a increased overweight/obesity risk [OR (95%CI):5.59(2.20-14.19)],[OR (95%CI):4.00(1.71-9.36)],and [OR (95%CI):3.08(1.10-8.68)]. The joint action of C1431T/-11377C>G was smaller than the single effect of-11377C>G genotype.12. There was an interaction between C1431T and-11377C>G genotype to hypertriglyceride. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased hypertriglyceride risk [OR (95%CI):3.73(1.42-9.82)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with hypertriglyceride risk. Compared to those with C1431T(CC)/-11377C>G(CC), the genotype of C1431T (CC)/-11377C>G(CG/GG),(CT/TT)/CC and (CC)/(CG/GG) had a increased hypertriglyceride risk [OR (95%CI):3.57(1.50-8.49)],[OR (95%CI):2.79(1.30-5.98)],and [OR (95%CI):2.45(0.97-6.22)]. The joint action of C1431T/-11377C>G was smaller than the single effect of-11377C>G genotype.13. There was not an interaction between C1431T and-11377C>G genotype to low HDL. However, In CC genotype of C1431T, children with CG/GG genotype of-11377C>G had an increased low HDL risk [OR (95%CI):3.43(1.33-8.91)]. In CC genotype of C1431T, children with CG/GG genotype of-11377C>G was not associated with hypertriglyceride risk.Conclusions1. CG/GG genotype of-11377C>G (rs266729) was associated with an increased metabolic syndrome risk. Polymorphisms of Pro12Ala rs1801282and C1431T (rs38568061) was not associated with metabolic syndrome.2. Sufficient physical activity had a decreased metabolic syndrome and its components risk.4. CG/GG genotype of-11377C>G (rs266729) was associated with an increased high blood pressure and overweight/obesity risk. Polymorphisms of Pro12Ala (rs1801282) and C1431T (rs38568061) was not associated with the components of metabolic syndrome.3. There were interaction between C1431T and-11377C>G genotype to metabolic syndrome and blood pressure, high waist circumference, hypertriglyceride, and overweight/obesity. The joint action of C1431T/-11377C>G was smaller than the single effect of-11377C>G genotype.4. There were interaction between physical activity and-11377C>G genotype to metabolic syndrome. |
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