Wei Qi, Jacobs David R, Schreiner Pamela J, Siscovick David S, Steffes Michael W, Fornage Myriam
Institute of Molecular Medicine, The University of Texas Health Science Center-Houston, 1825 Pressler St., Houston, TX 77030, USA.
J Mol Med (Berl). 2006 Nov;84(11):955-65. doi: 10.1007/s00109-006-0088-7. Epub 2006 Sep 6.
We performed a combination of single-variant- and haplotype-based analyses to investigate the association of peroxisome-proliferator-activated receptor gamma (PPARgamma) gene sequence variation with indices of adiposity, including body mass index (BMI) and waist girth, as well as insulin action, including fasting blood glucose and insulin levels. Nine polymorphisms, selected based on race-specific pairwise linkage disequilibrium relations and/or potential functional relevance, were assayed in 3,875 African-American and white young adults from the Coronary Artery Risk Development in Young Adults Study. These polymorphisms were C25819G (C-681G), C65746G (Pro12Ala), G67222A, A69208G, G81556T, T95872C, T115432G, C127599T, and C148157T (C1431T). They defined seven and six common haplotypes in African-Americans and whites, respectively. Patterns of associations of PPARgamma genetic variation with the metabolic traits differed between the two racial groups, with some exceptions. Haplotype CCGGCTCC was associated with a significant reduction in glucose levels in both racial groups (P<0.001 in each group), and the G69208 allele was associated with lower glucose levels in lean African-Americans and in whites (both P=0.02). Two haplotypes, relatively unique to whites, were associated with measures of adiposity and glucose levels. Two haplotypes, relatively unique to African-Americans, were associated with glucose levels. There were no significant effects of PPARgamma haplotypes on measures of body size in this racial group, but a novel polymorphism, G67222A, significantly modulated the relation between BMI and glucose levels (P interaction, 0.003). This study provides evidence that variants, other than Pro12Ala, influence variation in body size and indices of insulin action. It underscores the role of genetic and environmental contexts in shaping the patterns of associations of PPARgamma sequence variants with metabolic traits in human populations.
我们进行了基于单变异体和单倍型的联合分析,以研究过氧化物酶体增殖物激活受体γ(PPARγ)基因序列变异与肥胖指标(包括体重指数(BMI)和腰围)以及胰岛素作用指标(包括空腹血糖和胰岛素水平)之间的关联。基于种族特异性的成对连锁不平衡关系和/或潜在功能相关性,从青年动脉粥样硬化风险发展研究中选取了9个多态性位点,对3875名非裔美国人和白人青年进行了检测。这些多态性位点分别为C25819G(C-681G)、C65746G(Pro12Ala)、G67222A、A69208G、G81556T、T95872C、T115432G、C127599T和C148157T(C1431T)。它们在非裔美国人和白人中分别定义了7种和6种常见单倍型。PPARγ基因变异与代谢性状的关联模式在两个种族群体中有所不同,但也有一些例外。单倍型CCGGCTCC在两个种族群体中均与血糖水平显著降低相关(每组P<0.001),并且G69208等位基因与瘦的非裔美国人和白人的较低血糖水平相关(均为P=0.02)。两种相对白人特有的单倍型与肥胖和血糖水平指标相关。两种相对非裔美国人特有的单倍型与血糖水平相关。在这个种族群体中,PPARγ单倍型对体型指标没有显著影响,但一个新的多态性位点G67222A显著调节了BMI与血糖水平之间的关系(P相互作用=0.003)。这项研究提供了证据,表明除了Pro12Ala之外的变异体影响体型变异和胰岛素作用指标。它强调了遗传和环境背景在塑造PPARγ序列变异与人类群体代谢性状关联模式中的作用。