Maternal paraben exposure may contribute to childhood overweight development by altered pro-opiomelanocortin (POMC)-mediated neuronal appetite regulation, suggest the findings of a review of data from a mother-child cohort as well as outcomes with experimental approaches.
Childhood obesity cannot be explained by excessive food intake and sedentary behaviour alone. Parabens, a class of endocrine disruptive chemicals (EDC) that are added to cosmetics as preservatives or antimicrobials, can cross the blood-placenta barrier and influence prenatal development.
Within the LINA study, 629 mother-child pairs were recruited. Urinary concentration of butylparaben (BuP) during pregnancy were assessed, and a correlation between paraben urinary concentration and overweight children aged 2-8 years was reported. Weight increase was more evident in girls.
In vivo experiments on human and murine paraben exposed adipocytes showed decreased leptin and increased adiponectin secretion. Female mice that were exposed to BuP during gravity showed a significantly higher weight and food intake than control animals over the entire observation period. This effect may be related to reduced leptin signalling that leads to an inappropriate satiety signalling and increased food intake.
Gene expression of the leptin receptor (lepr) and POMC are downregulated due to paraben exposure. Only the nPE1 regulatory region (that downregulates the gene POMC, strongly associated with food intake regulation) had increased DNA methylation, showing the epigenetic nature of paraben effect on food intake regulation