Epigenetics of metabolic syndrome

Abstract

The dramatic increase in global prevalence of metabolic disease is inexplicable when considering only environmental or only genetic factors, leading to the need to explore the possible roles of epigenetic factors. A great deal of progress has been made in this interdisciplinary field in recent years, with many studies investigating various aspects of the metabolic syndrome and its associated epigenetic changes. Rodent models of metabolic diseases have been particularly illuminating because of the ability to leverage tools such as genetic and environmental modifications. The current review summarizes recent breakthroughs regarding epigenetic markers in studies of obesity, Type II diabetes, and cardiovascular disease, the three major disorders associated with metabolic syndrome. We also discuss open questions and future directions for integrating genomic, epigenomic, and phenotypic big biodata toward understanding metabolic syndrome etiology.

Keywords: Type II diabetes; cardiovascular disease; chromatin; epigenetics; histone modifications; metabolic syndrome; methylation; non-coding RNA; obesity.

Fig. 1.

The metabolic syndrome is the result of complex and nonlinear interactions among environment, genetics, and epigenetics. These factors interact with each other in feedback loops, and studies aimed at understanding how they interact will shed light on metabolic syndrome etiology.