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代谢综合征特征的遗传方差共享:遗传力研究。

Shared genetic variance between the features of the metabolic syndrome: heritability studies.

机构信息

Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.

出版信息

Mol Genet Metab. 2011 Dec;104(4):666-9. doi: 10.1016/j.ymgme.2011.08.035. Epub 2011 Sep 8.

DOI:10.1016/j.ymgme.2011.08.035
PMID:21963081
Abstract

Heritability estimates of MetS range from approximately 10%-30%. The genetic variation that is shared among MetS features can be calculated by genetic correlation coefficients. The objective of this paper is to identify MetS feature as well as MetS related features which have much genetic variation in common, by reviewing the literature regarding genetic correlation coefficients. Identification of features, that have much genetic variation in common, may eventually facilitate the search for pleitropic genetic variants that may explain the clustering of MetS features. A PubMed search with the search terms "(metabolic syndrome OR insulin resistance syndrome) and (heritability OR genetic correlation OR pleiotropy)" was performed. Studies published before 7th July 2011, which presented genetic correlation coefficients between the different MetS features and genetic correlation coefficients of MetS and its features with adipose tissue-, pro-inflammatory and pro-thrombotic biomarkers were included. Nine twin and 19 family studies were included in the review. Genetic correlations varied, but were strongest between waist circumference and HOMA-IR (r(2): 0.36 to 0.79, median: 0.50), HDL cholesterol and triglycerides (r(2): -0.05 to -0.59, median -0.45), adiponectin and MetS (r(2): -0.32 to -0.43; median -0.38), adiponectin and insulin (r(2): -0.10 to -0.60; median -0.30) and between adiponectin and HDL-cholesterol (r(2): -0.22 to -0.51, median -0.29). In conclusion, heritability studies suggest that genetic pleiotropy exist especially between certain MetS features, as well as between MetS and adiponectin. Further research on actual genetic variants responsible for the genetic pleiotropy of these combinations will provide more insight into the etiology of MetS.

摘要

代谢综合征的遗传度估计约为 10%-30%。可以通过遗传相关系数来计算代谢综合征特征之间共享的遗传变异。本文的目的是通过回顾有关遗传相关系数的文献,确定代谢综合征特征以及具有大量共同遗传变异的代谢综合征相关特征。鉴定具有大量共同遗传变异的特征,最终可能有助于寻找可能解释代谢综合征特征聚类的多效遗传变异。使用术语“(代谢综合征或胰岛素抵抗综合征)和(遗传度或遗传相关或多效性)”进行了 PubMed 搜索。纳入了发表于 2011 年 7 月 7 日之前、报告了不同代谢综合征特征之间遗传相关系数以及代谢综合征及其特征与脂肪组织、促炎和促血栓形成生物标志物之间遗传相关系数的研究。本综述共纳入 9 项双胞胎研究和 19 项家系研究。遗传相关性存在差异,但腰围和 HOMA-IR 之间最强(r(2):0.36-0.79,中位数:0.50),HDL 胆固醇和甘油三酯之间(r(2):-0.05 至-0.59,中位数-0.45),脂联素和代谢综合征之间(r(2):-0.32 至-0.43;中位数-0.38),脂联素和胰岛素之间(r(2):-0.10 至-0.60;中位数-0.30)以及脂联素和 HDL 胆固醇之间(r(2):-0.22 至-0.51,中位数-0.29)。总之,遗传度研究表明,遗传多效性尤其存在于某些代谢综合征特征之间,以及代谢综合征和脂联素之间。进一步研究导致这些组合遗传多效性的实际遗传变异将为代谢综合征的病因提供更多的见解。

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