Abstract
The prevalence of obesity has been increasing markedly in the U.S. and worldwide in the past decades; and notably, the obese populations are signified by not only the overall elevated adiposity but also particularly harmful accumulation of body fat in the central region of the body, namely, abdominal obesity. The profound shift from “traditional” to “obesogenic” environments, principally featured by the abundance of palatable, energy-dense diet, reduced physical activity, and prolonged sedentary time, promotes the obesity epidemics and detrimental body fat distribution. Recent advances in genomics studies shed light on the genetic basis of obesity and body fat distribution. In addition, growing evidence from investigations in large cohorts and clinical trials has lent support to interactions between genetic variations and environmental factors, e.g., diet and lifestyle factors, in relation to obesity and body fat distribution. This review summarizes the recent discoveries from observational studies and randomized clinical trials on the gene–environment interactions on obesity and body fat distribution.
Highlights
The past few decades have seen a rapid increase in the prevalence of obesity in the United States and worldwide [1,2]
The purpose of the current review is to summarize the recent findings of gene–environment interactions in relation to obesity and body fat distribution from observational studies and randomized clinical trials
Our current understanding about how these genetic factors interact with environmental factors, especially the underlying mechanisms, is still extremely lacking
Summary
The past few decades have seen a rapid increase in the prevalence of obesity in the United States and worldwide [1,2]. Body fat distribution is associated with risks of type 2 diabetes, coronary heart disease, and all-cause mortality, independent of overall adiposity as measured by BMI [7,8,9,10,11]. Many genes have been identified to be associated with obesity and body fat distribution, there is a growing consensus that the genetic variants with modest effects discovered by GWAS do not account for a large proportion of estimated heritability of obesity and body fat distribution Such missing heritability may at least partly be explained by the gene–environment interaction, which is not explicitly modeled in GWAS [21,22]. The review briefly discusses other omics studies on body fat distribution, challenges in this field, and future directions
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