Early-life perfluorooctanoic acid exposure induces obesity in male offspring and the intervention role of chlorogenic acid.

Perfluorooctanoic acid (PFOA) is an emerging organic pollutant (EOP) hazardous to human health. Effects of maternal PFOA exposure on offspring as well as the underlying mechanisms remain unclear. In this study, ICR mouse models of gestational low PFOA exposure (0.05 mg/kg/day) were established to investigate the roles on metabolic disorders of offspring. Body weight, body composition, hepatic lipid levels, transcriptome and metabolome were analyzed. Expression of genes related to lipid metabolism, inflammasome formation and gut barrier integrity were measured. Furthermore, oral administration of chlorogenic acid (CGA) (100 mg/kg/day) was performed to observe the rescue effect on lipid disorders caused by PFOA exposure. Our findings demonstrated that gestational exposure to PFOA resulted in obesity, hepatic inflammation, disorders of lipid metabolism, and disruption of gut barrier integrity in male offspring. Notably, these adverse effects were attenuated by CGA supplementation. These data suggested that PFOA exposure during early life stage induced potential risks for later onset of obesity and metabolic disorder which could be ameliorated by CGA treatment.