The fat tail of obesity as told by the genome
The fat tail of obesity as told by the genome
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DOI：
10.1097/mco.0b013e3283034990
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发表时间：
2008-07-01
影响因子：
3.1
通讯作者：
Herbert, Alan
中科院分区：
文献类型：
--
作者：
Herbert, Alan
综述的目的许多基因影响导致肥胖和预防肥胖的途径。我们询问有多少种不同的变异影响人类肥胖以及它们有多常见？最新发现当前一代全基因组关联扫描的能力中等，可以检测和复制单核苷酸多态性或常见拷贝数变异与常见疾病之间的关联。它们的设计目的不是为了发现罕见的种系变异或个体特有的、在成体干细胞中高频率出现的体细胞变化。他们不直接分析与母亲或环境暴露相关的结果的表观遗传重编程。总结与目前的全基因组关联扫描研究可以验证的相比，导致肥胖的基因变异、基因-基因和基因-环境相互作用更多。这些可验证的遗传关联为了解导致人类肥胖的途径提供了有价值的见解。
Purpose of reviewMany genes affect pathways that predispose to and protect against obesity. We ask how many different variants affect human obesity and how common are they?Recent findingsThe current generation of genome-wide association scans is moderately powered to detect and replicate associations between single nucleotide polymorphisms, or common copy number variations and common diseases. They are not designed either to find rare germline variants or those somatic changes, unique to an individual, that arise with high frequency in adult stem cells. They do not directly assay the epigenetic reprogramming of outcomes related to maternal or environmental exposures.SummaryThere are more gene variants, more gene-gene and gene-environmental interactions leading to obesity than current genome-wide association scan studies can verify. Those genetic associations that can be validated provide valuable insight into the pathways contributing to human obesity.