The rapid increase in the incidence and prevalence of obesity and metabolic syndrome over the last decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal environment also strongly influences the risk of developing such diseases in later life. One of the principal environmental factors influencing the developing child is nutrient availability, which is dependent on maternal nourishment status and placental functionality. The influence of a nutritional insult to the fetus will not only depend on the type of maternal nutritional insult but will also depend on the maternal metabolic condition, the timing of maternal nutritional insult, and will occur when there is a mismatch between pregnancy and postnatal environments. Both human and animal studies have shown that maternal under- (caloric restriction, protein restriction or micronutrient restriction) or overnutrition (high-fat, high-carbohydrate or high-vitamin diets) can induce persistent changes in gene expression and metabolism in the offspring, resulting in an increased risk for obesity and metabolic disease. Because these changes are mediated by altered epigenetic regulation of specific genes, and given that epigenetic marks are reversible, nutritional or pharmaceutical interventions may be used to modify long-term obesity and cardio-metabolic disease risk.
Keywords: Caloric restriction, Developmental programming, DNA methylation, Epigenetics, Famine, Folic acid, High-fat diet, High-sugar diet, Histone modifications, Maternal nutrition, Metabolic syndrome, Non-coding RNA, Obesity, Pregnancy, Protein-restriction.