The Study On The Association Of Peroxisome Proliferation-activated Receptor-delta+294T/C Gene Polymorphism With Lipid And Glucose Metabolism And Coronary Heart Disease

Objective Peroxisome proliferator-activated receptor-delta (PPARδ)is an ubiquitously expressed transcription factor that has been implicated in the regulation of genes related to lipid and glucose metabolism; The 4+294T/C polymorphism in PPARδrepresents a functional SNP affecting transcriptional activity of thePPARδgene.The study is To investigate the relationships of peroxisome proliferation-activated receptor-delta +294T/C gene polymorphisms with lipid glucose and metabolism , coronary heart disease (CHD).Methods 202 kinless subjects of the Chinese Han were investigated in this study, including 82 normal controls(NC) and 120 cases diagnosed as CHD with coronary angiography. Fasting blood glucose( FBG), plasma lipid(TG,TC,LDL-C,VLDL-C,HDL-C)levels were measured using fully-automatic biochemistry analysis apparatus. Fasting insulin( FINS)was measured using radioimmunity approach. Homeostasis model assessment estimate of insulin resistance (HOMA-IR) was computed with fasting insulin and fasting blood glucose. Body height and weight were determined for computing body mass index (BMI). PPARδ+294T/C gene polymorphisms were determined by polymerase chain reaction and restriction fragment length polymorphisms. The frequencies of PPARδ+294T/C genotypes and the C allele frequency were analyzed to evaluate clinical data, biochemical indicators and the risk of CHD among variant genotypes.Results (1) Fasting blood glucose was not significantly different in the variant genotypes of the CHD group; Fasting blood glucose was not significantly different in the variant genotypes of the NC group. (2) Fasting plasma lipids were not significantly different in the variant genotypes of the CHD group; Fasting plasma lipids were not significantly different in the variant genotypes of the NC group. (3) Homeostasis model assessment estimate of insulin resistance was not significantly different in the variant genotypes of the CHD group; Homeostasis model assessment estimate of resistance was not significantly different in the variant genotypes of the NC group. (4) BMI was not significantly different in the variant genotypes of the CHD group; BMI was not significantly different in the variant genotypes of the NC group. (5) The genotype distribution was significantly different between the CHD and the NC (P <0.05, +294TT 44.2% versus 62.2%, +294TC 50.0% versus 36.6%, +294CC 5.8% versus 1.2%, respectively). The frequencies of TC+CC genotype and C allele were evidently higher in the CHD group than those in the NC( P <0.05, 55.8%versus 37.8%, 30.8%versus 19.5%, respectively). Multivariate logistic regression analysis showed the CHD risk of the C allele carriers was significantly higher than that of the TT homozygote (C allele OR:2.74, 95 % CI:1.19～6.34).Conclusions (1) The data suggested that the PPARδ+294T/C polymorphism had no influence on FBG, plasma lipids levels, HOMA-IR and BMI . (2) There was evident association between PPARδ+294T/C gene polymorphisms and CHD, the C allele may be one of the risk factors of CHD.