| Description en | Obesity is increasing exponentially. Today, 20% of the school-aged children are overweight. The risk of becoming obese is influenced not only by genetic and adult life-style factors, but also by nutrition during pregnancy and infancy. This phenomenon is called metabolic programming. Animal studies have shown that a diet rich in methyl-group donors (e.g. folic-acid, folate, methionine, betaine, and choline) during pregnancy can reduce the risk of obesity in the offspring. These nutrients can influence our epigenome (e.g. DNA methylation pattern) and alter gene expression. In addition, early life exposure to endocrine disrupting chemicals (EDCs) might perturb neuro-endocrine systems involved in growth, energy metabolism, appetite, adipogenesis and glucose-insulin homeostasis and increase the risk of childhood obesity. We will investigate whether methyl-group donor intake and exposure to EDCs in early life will result in DNA methylation changes in genes related to obesity and will affect the risk of childhood obesity. If an effect of diet and exposure to EDCs should be established, this would create an enormous potential for preventive intervention with a tremendous health benefit for every citizen.
|
|---|
