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

被引:15
作者
Lu, Jing [1 ]
Huang, Guoren [1 ]
Hu, Sizhuo [1 ]
Wang, Zhenning [1 ]
Guan, Shuang [1 ]
机构
[1] Jilin Univ, Dept Food Qual & Safety, Changchun 130023, Peoples R China
关键词
1,3-DCP; Hyperlipidemia; AMPK signaling pathway; In vivo; ACTIVATED PROTEIN-KINASE; METABOLIC SYNDROME; ENERGY-METABOLISM; ADIPOSE-TISSUE; RISK-FACTORS; PPAR-ALPHA; LIVER; RATS; CHLOROPROPANOLS; OBESITY;
D O I
10.1016/j.fct.2013.11.049
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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 1 mg/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 (0.1-1 mg/kg/day) decreased p-AMPK/tAMPK ratio, p-ACC/tACC ratio, PPAR alpha 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. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:403 / 409
页数:7
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