Epigenetic events associated with obesity and diabetes

Abstract

Obesity is becoming a major public health concern. During the last years, genetic and epigenetic factors have been supposed to contribute to increase (or decrease) the susceptibility to gain weight and to develop obesity-related comorbidities. Metabolic syndrome, defined by a combination of disturbed glucose and insulin metabolism, central obesity, dyslipidemia, and hypertension, is considered to be a risk factor for type 2 diabetes and cardiovascular disease. The role of genetic factors involved in the etiology of human obesity is beyond question. Moreover there is evidence that the current epidemic of obesity and diabetes is environmentally driven. Studies during the past decade have indicated that normal metabolic regulation during adulthood not only requires a good matching of energy intake with energy expenditure, but also is influenced by fetal and postnatal environments. Epidemiological studies and experimental models show that maternal nutritional constraint during pregnancy alters the metabolic phenotype of the offspring and that this can be passed to subsequent generations. Recent researches in a number of laboratories all over the world suggest the continuous increase in the environment and food chains of obesogens, above all of endocrine disruptors, i.e., chemicals that interfere with many homeostatic mechanisms, altering the regulation of energy balance, promoting fat accumulation, adipogenesis, and weight gain. Finally epigenetic marks could be useful to personalize nutrition, to early detect those individuals with more risk to develop metabolic disorders or to better respond to a treatment.