Epigenetic Modifications Induced by Nutrients in Early Life Phases: Gender Differences in Metabolic Alteration in Adulthood.

ABSTRACT

Metabolic chronic diseases, also named noncommunicable diseases (NCDs), are considered multifactorial pathologies, which are dramatically increased during the last decades. Noncommunicable diseases such as cardiovascular diseases, obesity, diabetes mellitus, cancers, and chronic respiratory diseases markedly increase morbidity, mortality, and socioeconomic costs. Moreover, NCDs induce several and complex clinical manifestations that lead to a gradual deterioration of health status and quality of life of affected individuals. Multiple factors are involved in the development and progression of these diseases such as sedentary behavior, smoking, pollution, and unhealthy diet. Indeed, nutrition has a pivotal role in maintaining health, and dietary imbalances represent major determinants favoring chronic diseases through metabolic homeostasis alterations. In particular, it appears that specific nutrients and adequate nutrition are important in all periods of life, but they are essential during specific times in early life such as prenatal and postnatal phases. Indeed, epidemiologic and experimental studies report the deleterious effects of an incorrect nutrition on health status several decades later in life. During the last decade, a growing interest on the possible role of epigenetic mechanisms as link between nutritional imbalances and NCDs development has been observed. Finally, because of the pivotal role of the hormones in fat, carbohydrate, and protein metabolism regulation throughout life, it is expected that any hormonal modification of these processes can imbalance metabolism and fat storage. Therefore, a particular interest to several chemicals able to act as endocrine disruptors has been recently developed. In this review, we will provide an overview and discuss the epigenetic role of some specific nutrients and chemicals in the modulation of physiological and pathological mechanisms.