WITHDRAWN: Could some epigenetic modifications hold the key to opposing the metabolic syndrome?

Abstract

// Giovanni Tarantino 1,2,* , Matteo Nicola Di Minno 1,* and Carmine Finelli 3,* 1 Department of Clinical Medicine and Surgery, Federico II University Medical School of Naples, Via Sergio Pansini, Naples, Italy 2 Centro Ricerche Oncologiche di Mercogliano, Istituto Nazionale Per Lo Studio E La Cura Dei Tumori “Fondazione Giovanni Pascale”, IRCCS, Italy, Italy 3 Department of Emergency and Internal Medicine, Ospedale S. Maria della Pieta – ASL Napoli 3 Sud, Nola (Na), Italy * These authors have contributed equally to this work Correspondence to: Giovanni Tarantino, email: // Keywords : non alcoholic fatty liver diseases, metabolic syndrome, epigenetics, microRNAs, PUFAs Received : January 27, 2016 Accepted : December 12, 2016 Epub : December 21, 2016 Abstract The role of epigenetic mechanisms in the pathogenesis of diseases has been increasingly recognized over recent years. Due to the intrinsic flexibility of the chromatin structure both in response to diet and environment, and as a result of foreseeable therapeutic interventions, epigenetics has emerged as a promising conceptual frame to investigate chronic degenerative disorders. This applies particularly to diet-driven and environment-driven metabolic disorders, such as obesity and its complications, including atherosclerosis and non-alcoholic fatty liver diseases (NAFLD). Current evidence strongly suggests that chronic inflammation is a landmark of obesity, atherosclerosis, and NAFLD, and that markers of inflammation are important predictors of cardiovascular risk factors. A crucial question is how pro-inflammatory gene expression patterns are established and maintained in the aforementioned illnesses. Epigenetic gene regulation is a partially new entry in the field of cardiovascular diseases. Epigenetic modifications provide attractive candidate disease mechanisms by explaining, in principle, how diet, environment and lifestyle might impose aberrant gene expression patterns in the individual’s lifetime, which can also be considered the result of trans-generational epigenetic inheritance. The main long-term goals in this field are to identify and understand the role of the epigenetic marks that could be used as early predictors of metabolic risk, and possibly develop drugs or diet-related treatments able to delay these epigenetic changes or even reverse them. Therefore, a continued and greater understanding of these mechanisms will eventually help identify individuals at high risk of the Metabolic Syndrome, and develop therapeutic interventions, in accordance with current global government strategy, utilizing also PUFA rich foods.