Economic development is associated with a nutrition transition process characterised by the consumption of highly processed food rich in energy at the expense of natural food containing large amounts of fibre and low amounts of sugar and fat. In turn, nutrition transition is correlated to an enhanced incidence of non-communicable diseases including obesity and metabolic syndrome which are major contributors to mortality rates all over the world. This shift from a pattern of high prevalence of infectious diseases to one of high prevalence of chronic and degenerative disorders, is termed Epidemiological Transition. This phenomenon has been explained by socioeconomic factors that condition the consumers choice of energy-rich food such that health policies to fight against the obesity epidemic are based almost exclusively on the promotion of physical exercise and the consumption of “healthy” food. Nevertheless, this approach fails to reduce body weight and improve health in a large percentage of the affected population. These negative results can be explained by the fact that in utero and neonatal nutrition determines also the susceptibility to develop metabolic diseases through a metabolic programming process. Actually, the offspring of obese mothers exhibit increased birth weight and are at enhanced risk of obesity and metabolic syndrome. Therefore, epidemiological transition is likely the combined result of the increased disease susceptibility induced by malnutrition during in utero and neonatal development and the detrimental influence of an obesogenic environment later in life driven by economic, social and cultural factors. However, few studies, if any, have analysed the interaction between the biological and socioeconomic determinants of obesity as the leading underlying cause of epidemiologic transition. This project aims at studying the biological and socio-economical determinants of obesity and metabolic disease risk in the offspring of obese mothers in two populations undergoing different rates of nutrition transition. We will search for interactions between one carbon/energy metabolism and metabolic and epigenomic marks in biological samples from French and Mexican mothers and their new-borns relevant to metabolic disease risk and analyze their correlation with socio-economic factors related to health disparities, food insecurity, maternal feeding patterns and infant feeding practices using a multilevel and socio-economical determinants approach. This analysis will be completed by an experimental study in an animal model of maternal obesity to determine whether, and how, the identified metabolic and epigenomic modifications in humans result in an altered control of energy metabolism and can be reverted by a nutritional intervention. Collectively, these studies should allow us to: 1) establish a causal multilevel model allowing to analyze the combined influence of socio-economic and maternal health and lifestyle factors on the risk of metabolic disease in their children; 2) get unique insights and an integrated view of the common and/or divergent socio-economic and biological factors in two populations experiencing different levels of nutrition transition that could explain health disparities and the risk of metabolic disease in infants born to obese mothers; 3) identify bio-markers in children with potential predictive value for the development of obesity and metabolic disease; 4) generate fundamental information relevant to the establishment of nutritional and lifestyle recommendations to women of child bearing age and to pregnant women and that could be used to the design of adapted diets to overcome the detrimental consequences on health of nutrition transition; 5) obtain fundamental scientific knowledge for a better understanding of the mechanisms underpinning the nutritional programming of metabolic disorders.