Obesity-Related Epigenetic Changes After Bariatric Surgery

Abstract

Objective: In recent years, an increasing number of studies have begun focusing on epigenetics as a link between environmental factors and a greater predisposition to the development of obesity and its comorbidities. An important challenge in this field is the evaluation of the possibility of the reversal of obesity-related epigenetic marks by means of therapy to induce weight loss and if the beneficial effects of therapy in reducing obesity are mediated by epigenetic mechanisms. We aimed to offer an outline of the current results regarding to the impact of bariatric surgery on epigenetic regulation, as well as to show if the beneficial effect of this intervention could be mediated by epigenetic mechanisms. Methods: A review of the scientific publications in PubMed was performed by using key words related to obesity, epigenetics and bariatric surgery to provide an update of recent findings in this area of research. The most relevant and recently published articles and abstracts were selected to frame this review. Results: Previous studies have demonstrated the presence of differential DNA methylation after bariatric surgery and the differential expression of non-coding RNAs. Therefore, epigenetic regulation could mediate the benefit of bariatric surgery on body weight and the metabolic disturbances associated with excess body weight, such as insulin resistance, hypertension, and cardiovascular disease. This evidence is relatively new as epigenetic regulation was first evaluated in the obesity field only a few years ago. However, there is an urgent need to perform longitudinal studies to evaluate the capacity of epigenetic marks in the prediction of bariatric surgery response. Conclusions: Bariatric surgery appears to be capable of partially reversing the obesity-related epigenome. The identification of potential epigenetic biomarkers predictive for the success of bariatric surgery may open new doors to personalized therapy for severe obesity.

Epigenetic contribution to obesity

“…2 ). Thus, several beneficial effects observed 1 year after the metabolic surgery on metabolism, immunity and inflammation appeared to be mediated by epigenetic mechanisms (Izquierdo and Crujeiras 2019 ). However, more longitudinal and large studies are needed because up to now only small cohorts were characterized.…”

The effects of bariatric surgery on clinical profile, DNA methylation, and ageing in severely obese patients

“…Epigenetic mechanisms are modifiable via environmental exposures and lifestyle factors, therefore, such a considerable change after bariatric surgery may have an impact on DNA methylation [62]. In this regard, it was proposed that epigenetic regulation could mediate the benefit of bariatric surgery on body weight and the metabolic disturbances associated with excess body weight, such as insulin resistance, hypertension, and cardiovascular disease [12].…”

“…The mechanisms underlying metabolic improvement after bariatric surgery are not fully understood yet, but epigenetic factors have been proposed to play a significant role [10,11]. This is because the obesity-related metabolic disturbances are produced as a result of an interaction between environmental, lifestyle, and genetic factors and epigenetics mediates the environmental effect on the cellular function of the organism [12]. One of the most studied epigenetic mechanisms is DNA methylation, which includes methyl group binding to the cytosines of cytosine-guanine dinucleotides (CpG sites) [13].…”

Integrative analyses of biomarkers and pathways for adipose tissue after bariatric surgery

“…Obesity has emerged as a worldwide epidemic with far-reaching, increasing, and negative impacts on morbidity from obesity and its co-morbidities that include type 2 diabetes (T2DM), cardiovascular disease (CVD), and several cancer types[ 1 ], and of course mortality [ 2 ]. The global number of obese individuals (age >5 years) increased from 74 to 440 million for females and 37–357 million in males from 1975 to 2016 [ 3 ].…”