The study by Barra et al. (66) is based on additional experiments to support this hypothesis, in one of those studies it was observed that the exposure of mice with genetic or pharmacological inhibition of ryptophan hydroxylase 1 (Tph1) to BPA, evaluated whether the metabolic deficits induced by BPA, such as obesity, depend on the production of peripheral serotonin, since peripheral serotonin in adipose tissue functions as an obesity hormone that reduces energy expenditure and increases lipid accumulation (67). This evidence concerns the gene TPH1 and Obesity.