Tehran University of Medical Sciences Iranian Journal of Public Health 2251-6085 47 7 2018 07 16 973 979 Chao SHEN Dept. of Epidemiology, School of Public Health, Medical College of Soochow University, Suzhou, China AND The Center for Disease Control and Prevention of Suzhou Industry Park, SuZhou, China Wei FAN Dept. of Epidemiology, School of Public Health, Medical College of Soochow University, Suzhou, China Hui-Jian XIE Dept. of Epidemiology, School of Public Health, Medical College of Soochow University, Suzhou, China Ming WU Center for Disease Control, Nanjing, Jiangsu Province, China Zheng-Yuan ZHOU Center for Disease Control of Changshu, Suzhou, China Zhi-Rong GUO Dept. of Epidemiology, School of Public Health, Medical College of Soochow University, Suzhou, China Chen DONG Dept. of Epidemiology, School of Public Health, Medical College of Soochow University, Suzhou, China 2018 07 16 2018 07 16   Background: Lipoprotein (a) [Lp(a)], as an independent risk factor for cardiovascular disease, is more likely to be genetically determined according to the increasing evidence of epidemiologic and clinical studies in recent years. Peroxisome proliferator-activated receptor (PPAR)γ, the ligand-activated transcription factors, was considered as an indispensable role in the process of lipid metabolism. This study was designed to explore the associations of three single-nucleotide polymorphisms (SNPs) and the haplotypes of the peroxisome proliferator-activated receptor (PPAR)γ gene with the level of Lp(a). Methods: Participants were recruited under the framework of the PMMJS (The Prevention of Metabolic Syndrome (MS) and Multi-metabolic Disorders in Jiangsu Province of China Study) from Apr 1999 to Jun 2004. Overall, 644 subjects were randomly selected and 3 SNPs of PPARγ gene (rs10865710, rs1805192, rs4684847) were genotyped. Results: After adjusting for age, sex, cigarette smoking, alcohol drinking, waist circumference and body mass index, rs4684847 was significantly associated with Lp (a). The presence of the rs4684847 T allele (CT+TT) have a lower level of Lp (a) than the allele (CC) in the dominant model, mean difference was -27.30 (95%CI:-52.88~-1.73) mg/L, P<0.05. G-P-T and G-A-T haplotype were associated with lower levels of Lp (a) (P=0.0041 and<0.0001), mean difference was 49.79(95%CI:-97.52~-2.06) mg/L and 17.75(95%CI:-25.75~-9.75) mg/L. Conclusion: PPAR gamma polymorphisms (rs10865710, rs1805192, rs4684847) and haplotypes may be the genetic risk factors for Lp (a) level.     https://ijph.tums.ac.ir/index.php/ijph/article/view/14041 https://ijph.tums.ac.ir/index.php/ijph/article/download/14041/6038