Abstract
A healthy diet improves life expectancy and helps to prevent common chronic diseases such as type 2 diabetes (T2D) and obesity. The mechanisms driving these effects are not fully understood, but are likely to involve epigenetics. Epigenetic mechanisms control gene expression, maintaining the DNA sequence, and therefore the full genomic information inherited from our parents, unchanged. An interesting feature of epigenetic changes lies in their dynamic nature and reversibility. Accordingly, they are susceptible to correction through targeted interventions. Here we will review the evidence supporting a role for nutritional factors in mediating metabolic disease risk through DNA methylation changes. Special emphasis will be placed on the potential of using DNA methylation traits as biomarkers to predict risk of obesity and T2D as well as on their response to dietary and pharmacological (epi-drug) interventions.
Highlights
Obesity and type 2 diabetes (T2D) are responsible for a major reduction in life expectancy and quality of life, increasing healthcare costs
While a genetic component undoubtedly plays a role in determining individual susceptibility to these traits, the genetic loci identified by genome-wide association studies (GWASs) only explain a small fraction of the heritability of these disorders [1,2]
Bacos et al [87] demonstrated that blood-borne epigenetic marks reflect age-related DNA methylation changes in human islets, and that altered methylation at certain genes are associated with the future insulin-secreting capacity and future risk of T2D
Summary
Obesity and type 2 diabetes (T2D) are responsible for a major reduction in life expectancy and quality of life, increasing healthcare costs. Genetic studies have so far left the issue of how metabolic disorders are transmitted unsolved These low heritability estimates, along with the dramatic increase in their worldwide prevalence, suggest a major role of lifestyle factors in these diseases [3]. Post-translational changes in histone proteins can alter the chromatin conformation and gene regulation, contributing to the metabolic disease phenotype Their influence on the development of obesity and T2D has been well-described elsewhere [6], and will not be covered in the present review, which is focused on DNA methylation. HFD replacement with a standard chow diet is accompanied by simultaneous improvement of the metabolic phenotype and rescue of normal methylation levels at Hoxa5 [15] All together, these findings have uncovered the capacity of epigenetics to adaptively respond to different nutritional conditions and suggest that targeting epigenetic plasticity may, in the future, offer novel and realistic opportunities to prevent and treat obesity and T2D. The potential use of DNA methylation marks in the evaluation of disease risk and efficacy of intervention will be discussed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
