Nonalcoholic fatty liver disease induced by 13-week oral administration of 1,3-dichloro-2-propanol in C57BL/6J mice

• 1,3-DCP (0.1–0.5 mg/kg/day) could induce NAFLD in C57BL/6J mice.
• 1,3-DCP induced NAFLD through dysregulation of AMPK signaling pathway.
• The NOAEL of 1,3-DCP was 0.01 mg/kg/day in C57BL/6J mice by oral administration.

1,3-Dichloro-2-propanol (1,3-DCP) is a food born chloropropanol contaminant that has been detected during the production process of a wide range of foods. In this study, we investigated the effect of 1,3-DCP on lipid metabolism of mice after 13-week subchronic exposure. The data showed that 1,3-DCP (0.05–0.5 mg/kg/day) could induce nonalcoholic fatty liver disease (NAFLD) in C57BL/6J mice and the NOAEL was 0.01 mg/kg/day. In addition, we studied the signaling pathway to see how 1,3-DCP worked. The data showed that NAFLD induced by 1,3-DCP was due to the dysregulation of AMPK signaling pathway. As far as we are aware, this is the first study to use 13-week subchronic toxicology to investigate the effect of 1,3-DCP on the development of NAFLD in mice. Our study provided evidence for diet contaminants in the development of NAFLD and furthered the safety evaluation of 1,3-DCP through subchronic exposure.

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