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The INSIG2 rs7566605 genetic variant does not play a major role in obesity in a sample of 24722 individuals from four cohorts

机译:在来自四个队列的24722名个体的样本中INSIG2 rs7566605遗传变异在肥胖中不发挥主要作用

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摘要

BackgroundIn a genome-wide association study performed in the Framingham Offspring Cohort, individuals homozygous for the rs7566605 C allele located upstream of insulin-induced gene 2 (INSIG2) were reported to incur an increased risk of obesity. This finding was later replicated in four out of five populations examined. The goal of the study reported here was to assess the role of the INSIG2 single nucleotide polymorphism (SNP) in susceptibility to obesity in the prospective longitudinal Atherosclerosis Risk in Communities (ARIC) study (n = 14,566) and in three other cohorts: the Coronary Artery Risk Development in Young Adults (CARDIA) study (n = 3,888), the Genetic Epidemiology Network of Arteriopathy (GENOA) study (n = 4,766), and extremely obese and lean individuals ascertained at the University of Ottawa (n = 1,502). The combined study sample is comprised of 24,722 white, African-American, and Mexican-American participants.
机译:背景技术在Framingham后代队列中进行的全基因组关联研究中,据报道位于胰岛素诱导基因2(INSIG2)上游的rs7566605 C等位基因纯合的个体患肥胖症的风险增加。此发现随后在五分之四的被检查人群中重复。此处报道的研究目的是在社区预期性纵向动脉粥样硬化风险(ARIC)研究(n = 14,566)和其他三个队列中评估INSIG2单核苷酸多态性(SNP)在肥胖易感性中的作用。年轻人的动脉风险发展(CARDIA)研究(n = 3,888),遗传疾病流行病学网络动脉病(GENOA)研究(n = 4,766),以及渥太华大学确定的极度肥胖和苗条的个体(n = 1,502)。合并的研究样本由24,722名白人,非洲裔美国人和墨西哥裔美国人组成。

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