Developmental programming of adulthood obesity and cardiovascular disease in the mouse by maternal nutritional imbalance

(eng) A link between early malnutrition and development of components of the metabolic syndrome later in life has been shown in epidemiological and animal data. Moreover, studies now tend to demonstrate that not only fetal environment is important for developmental programming but postnatal milieu could also participate to this process. The “predictive adaptive response” hypothesis stipulates that not only a suboptimal environment during fetal life will lead to development of metabolic disorders later in life but more likely is a mismatch between the early environment and that one really encountered later on that increases the risk of developing later disease. Based on this hypothesis, we examined the effect of an early mismatched environment produced by fetal protein restriction and postnatal catch-up growth on the development of obesity and cardiovascular disease in male mice. We focussed our study on the analysis of adipose tissue with in vitro examination of differentiation, proliferation of preadipocytes. We also investigated in vivo the development of overweight in adult mice and we measured the expression of specific adipose tissue molecules with microarray. Finally, we investigated the development of hypertension and atherosclerosis in parallel to obesity. Our results indicated that postnatal catch-up growth after fetal protein restriction favours the development of obesiy in adult male mice. Early mismatched nutrition also influenced the capacity of proliferation of preadipocyte as well as the expression of adipose tissue specific molecules involved mainly in lipid biosynthesis. Finally, early nutrition also induced hypertension in adult male mice while no influence of fetal protein restriction and postnatal catch-up growth was observed on atherosclerosis development.