Department of Biochemistry and Molecular Biology, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA.
Curr Genomics. 2011 May;12(3):180-9. doi: 10.2174/138920211795677903.
Childhood overweight and obesity have reached epidemic proportions worldwide, and the increase in weight-associated co-morbidities including premature type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease will soon become major healthcare and economic problems. A number of studies now indicate that the childhood obesity epidemic which has emerged during the past 30 years is a complex multi-factorial disease resulting from interaction of susceptibility genes with an obesogenic environment. This review will focus on gene-diet interactions suspected of having a prominent role in promoting childhood obesity. In particular, the specific genes that will be presented (FTO, MC4R, and NPC1) have recently been associated with childhood obesity through a genome-wide association study (GWAS) and were shown to interact with nutritional components to increase weight gain. Although a fourth gene (APOA2) has not yet been associated with childhood obesity, this review will also present information on what now represents the best characterized gene-diet interaction in promoting weight gain.
儿童超重和肥胖已在全球范围内达到流行程度，与体重相关的合并症（包括 2 型糖尿病和动脉粥样硬化性心血管疾病）的发病率增加，很快将成为主要的医疗保健和经济问题。现在有许多研究表明，过去 30 年来出现的儿童肥胖症流行是一种复杂的多因素疾病，是由易感基因与致肥胖环境相互作用引起的。这篇综述将重点关注可能在促进儿童肥胖方面起重要作用的基因-饮食相互作用。特别是，本文将介绍的特定基因（FTO、MC4R 和 NPC1）最近通过全基因组关联研究（GWAS）与儿童肥胖相关，并显示与营养成分相互作用以增加体重增加。虽然第四个基因（APOA2）尚未与儿童肥胖相关，但本文还将介绍目前促进体重增加的特征最明确的基因-饮食相互作用的信息。
