1,3-Dichloro-2-propanol induced hyperlipidemia in C57BL/6J mice via AMPK signaling pathway

[Display omitted] •1,3-DCP (0.1–1mg/kg/day) did not affect food intake and body weight of C57BL/6J mice.•1,3-DCP (0.1–1mg/kg/day) increased serum TC, TG and LDL-C, decreased HDL-C in mice.•1,3-DCP (0.1–1mg/kg/day) increased relative liver weight, hepatic TG and TC in mice.•1,3-DCP (0.1–1mg/Kg/day) increased adipose tissue weight and adipocyte size in mice.•1,3-DCP induced hyperlipidemia at least partially through AMPK signaling pathway. 1,3-Dichloro-2-propanol (1,3-DCP) is a well-known contaminant that has been detected in a wide range of foods. Dietary intake represents the greatest source of exposure to 1,3-DCP. In the study, we first found 1,3-DCP could induce hyperlipidemia in C57BL/6J mice below 1mg/kg/day. We investigated serum lipid profile, liver total cholesterol (TC) and triglyceride (TG), histopathology of Liver and adipose tissue. The results showed 1,3-DCP dose dependently increased serum TG, TC and low-density lipoprotein cholesterol (LDL-C), decreased serum high-density lipoprotein cholesterol (HDL-C), increased relative liver weight, liver TG and TC, relative adipose tissue weight and enlarged the size of adipose cells. Because AMPK signal pathway is important in the process of lipid metabolism, we further investigated the effects of 1,3-DCP on AMPK signaling pathway in murine models. The results showed that 1,3-DCP (0.1–1mg/kg/day) decreased p-AMPK/tAMPK ratio, p-ACC/tACC ratio, PPARα expression, but increased FAT, SREBP1, HMGCR and FAS expression. These observations indicated that 1,3-DCP induced hyperlipidemia in C57BL/6J mice at least partially through regulating AMPK signaling pathway.