Perinatal exposure to chlorpyrifos and/or a high-fat diet is associated with liver damage in male rat offspring.

Abstract

Metabolic impairments in childhood are known to promote the development of type 2 diabetes and/or obesity in adulthood. These impairments may result from perinatal exposure to harmful environmental factors, such as pesticide residues or the consumption of a "western" diet. In the present study, we sought to determine whether an obesogenic profile, metabolic disorders and liver damage in offspring (observed during young adulthood) were related to maternal exposure to the pesticide chlorpyrifos (CPF) and/or a high-fat diet (HFD) starting 4months before conception and ending at weaning. After the end of exposure, 51 male rat pups were left to develop under normal conditions and were studied in young adulthood. Despite the absence of direct exposure to harmful factors (other than through the dam's milk), maternal exposure to CPF or an HFD was associated with changes in the offspring's metabolic activity in the liver in the offspring. This indirect exposure to CPF was associated with a relative reduction in the expression of genes coding for enzymes involved in lipid or glucose metabolism but did induce histopathological changes in the offspring at adulthood. Maternal exposure to an HFD alone or to CPF alone gave similar results in offspring, changes in the same direction. Exposure of the mother to HFD did not exacerbate CPF effects. Co-exposure to both CPF and HFD did not increase the observed effects compared to each factor taken separately.