Obesity and metabolic syndrome are increasing epidemic worldwide, especially in developed countries. Obesity and metabolic disease increase the risk of suffering certain diseases such as diabetes, cardiovascular disease, NASH, neurodegenerative disorders or some type of cancers like colorectal cancer. Adipose tissue is nowadays considered as an important organ that can regulate body homeostasis and modulate other tissues function through the delivery of a wide range of molecules. It has been shown that in obesity and metabolic disease context an adipose tissue dysfunction exists, producing changes in the adipokine secretion profile that in turn can prone to the disorders usually associated to these conditions. Besides, metabolic disease and obesity development are closely related to environmental factors such as food, smoking, sedentary habits, etc. However, obesity and metabolic syndrome also have a genetic and an epigenetic component, being regarded the epigenetic landscape as a mediator between environmental and genetic factors.
In this sense, epigenetics mechanisms can be shaped by nutrition, smoking or exercise among other lifestyle factors. There are two main epigenetics mechanism: 1) DNA methylation, which occurs in the C5 of a cytosine pyrimidine near to a guanine (position called CpG); and 2) histone modifications, which mainly occurs in the N terminal of histone proteins and that have a more diverse nature (acetylation, methylation, phosphorylation, sumoylation, ubiquitination, glycosylation,…). Both mechanism have been shown to be deregulated in metabolic syndrome and obesity, and could be implied in the etiology and associated risks observed in these conditions.
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