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.
