Gene–Lifestyle Interactions in Obesity

Jana V Van Vliet-Ostaptchouk,Vasiliki Lagou,Harold Snieder

doi:10.1007/s13668-012-0022-2

Abstract

Obesity is a complex multifaceted disease resulting from interactions between genetics and lifestyle. The proportion of phenotypic variance ascribed to genetic variance is 0.4 to 0.7 for obesity and recent years have seen considerable success in identifying disease-susceptibility variants. Although with the advent of genome-wide association studies the list of genetic variants predisposing to obesity has significantly increased the identified variants only explain a fraction of disease heritability. Studies of gene–environment interactions can provide more insight into the biological mechanisms involved in obesity despite the challenges associated with such designs. Epigenetic changes that affect gene function without DNA sequence modifications may be a key factor explaining interindividual differences in obesity, with both genetic and environmental factors influencing the epigenome. Disentangling the relative contributions of genetic, environmental and epigenetic marks to the establishment of obesity is a major challenge given the complex interplay between these determinants.

Highlights

Obesity was once considered a problem of economically developed countries, but the number of overweight and obese people is dramatically increasing in low- and middleincome countries at a rate never seen before [1]
It is widely accepted that multiple factors contribute to this epidemic, including economic growth, modernization, urbanization and, most importantly, changes in our lifestyle, as eating habits have shifted to greater consumption of energy-dense foods that are high in fats and sugars, while at the same time, physical activity has decreased [1, 3]
AA African American; BF% body fat percentage; BMI body mass index; CVD cardiovascular disease; EA European American; GEI gene–environment interaction; GI glycemic index; PA physical activity; PUFA polyunsaturated fatty acid; SAT subcutaneous fat; SFA saturated fatty acid; SNP single-nucleotide polymorphism; TF total fat; VAT visceral fat; WC waist circumference peroxisome proliferator-activated receptor-γ (PPARγ) gene, which has been extensively studied for GEI related to obesity and type 2 diabetes [32, 43], was reported to have a dietrelated effect on risk to obesity with the Pro12 allele being associated with increased adiposity in a high-fat diet group [44]

Summary

Introduction

Obesity was once considered a problem of economically developed countries, but the number of overweight and obese people is dramatically increasing in low- and middleincome countries at a rate never seen before [1]. To provide an overview on the most current publications in relationship to GEI in obesity, we searched PubMed (February 15, 2012) using a combination of keywords for genetic studies (i.e. gene, genetic variant, polymorphism, SNP), different obesityrelated phenotypes (i.e. overweight, obesity, BMI, waist, hip, WHR, fat, adiposity) and environmental factors (i.e. feeding, diet, physical activity, alcohol, smoking, stress).

Results

Conclusion