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Purpose adiponectin, tumor necrosis factor-α (TNF-α) levels and genetic polymorphisms related to childhood obesity, the paper analyzes the changes in obese children plasma adiponectin and TNF-α and obesity-related indicators The relationship further analysis of the adiponectin gene 45 points and TNF-α gene -308 single nucleotide polymorphism (SNP) in the distribution of the frequency of normal and obese children, and explore both SNP and childhood obesity relationship. Obese children 147 were obese group randomly selected from Kaifu District, Changsha City elementary school, elect the age-and sex-matched normal weight children 118 human normal control group were detected Height, weight, waist circumference (WC), hip circumference (HC), contraction pressure (SBP) and diastolic blood pressure (DBP), dual-energy X-ray absorption method detects body fat percentage (?), the automatic biochemical assay serum triglyceride (TG), total cholesterol (TC), high density lipoprotein ( HDL-C) and low-density lipoprotein (LDL-C), glucose oxidase test fasting plasma glucose (FPG), were measured by radioimmunoassay, fasting insulin (FINS) level, measured by ELISA adiponectin and TNF-α levels to calculate body mass index (BMI), waist-to-hip ratio (WHR) and insulin resistance index (HOMA-IR). Polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) methods detect adiponectin gene 45 points and TNF-α gene -308 polymorphism, randomly select the part of the sample application direct sequencing of PCR validation -RFLP results. The application of single-factor analysis of variance, chi-square test, linear correlation analysis and multiple regression analysis were statistically analyzed. 1, children of obese children adiponectin levels were lower than normal group (P lt; 0.05), and TNF-α, BMI, WHR, of HOMA-IR,?, FINS, SBP, TG was negatively correlated (P lt ; 0.05); obese children TNF-α levels higher than children in the normal group (P lt; 0.01), and BMI, WHR? FINS, HOMA-IR, TG, SBP was a significant positive correlation (P lt; 0.01) HDL (P lt; 0.05) was negatively correlated; stepwise multiple regression analysis showed that adiponectin, TNF-α, FINS and HOMA-IR? influencing factors, and adiponectin in the body and TNF-α level interaction statistically significant. 2, adiponectin gene SNP 45 in the frequency of occurrence of obese children and normal groups were 40.5% and 25.4%, respectively, between the two groups of allele and genotype frequencies were statistically significant (all P lt; 0.01) obese children G allele frequency was significantly higher than the normal group (OR = 2.00,95% CI 1.37-2.90); obese children and found the TT genotype and TG, GG-high adiponectin levels, and? TC and LDL-C level is low. TNF-α gene SNP-308 obese group and the normal group A allele mutation rate were 10.6% and 6.8%, respectively, between the two groups of genes and genotype frequencies not statistically significant (all P gt; 0.05); against obesity Children in the adiponectin gene SNP 45 and TNF-α gene SNP-308 related analysis, both correlation (P lt; 0.01, C = .2910). Conclusions of obese children in adiponectin levels of TNF-α levels rise, both in vivo interaction involved in the occurrence of obesity; adiponectin gene SNP 45 associated with the incidence of childhood obesity, T → G mutations increase childhood obesity the occurrence of disease incidence risk; no correlation of TNF-α gene SNP-308 and the incidence of childhood obesity; obese children gene single nucleotide polymorphisms can influence each other.
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