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

被引：3

作者：

Lu, Jing ^{[1
,2
]}

Fang, Baochen ^{[1
]}

Ren, Mengrou ^{[1
]}

Huang, Guoren ^{[1
]}

Zhang, Shuang ^{[1
]}

Wang, Yi ^{[1
]}

Deng, Xuming ^{[2
]}

Guan, Shuang ^{[1
,2
]}

机构：

[1] Jilin Univ, Dept Food Qual & Safety, Changchun 130062, Jilin, Peoples R China

[2] Jilin Univ, Minist Educ, Key Lab Zoonosis Res, Changchun 130062, Jilin, Peoples R China

来源：

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2015年 / 39卷 / 03期

关键词：

NAFLD; 1,3-DCP; Subchronic toxicity; AMPK; PATHWAY; BINDING; KINASE; FOOD; RATS;

D O I：

10.1016/j.etap.2015.04.007

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

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. (C) 2015 Elsevier B.V. All rights reserved.

引用

页码：1115 / 1121

页数：7

共 23 条

[1] LKB1-dependent signaling pathways [J].

Alessi, Dario R. ;

Sakamoto, Kei ;

Bayascas, Jose R. .

ANNUAL REVIEW OF BIOCHEMISTRY, 2006, 75 :137-163

[2]

AlKhater S. A., 2015, OBES REV

[3] Toxicology, occurrence and risk characterisation of the chloropropanols in food: 2-Monochloro-1,3-propanediol, 1,3-dichloro-2-propanol and 2,3-dichloro-1-propanol [J].

Andres, Susanne ;

Appel, Klaus E. ;

Lampen, Alfonso .

FOOD AND CHEMICAL TOXICOLOGY, 2013, 58 :467-478

[4] Deriving a data-based interspecies assessment factor using the NOAEL and the benchmark dose approach [J].

Bokkers, Bas G. H. ;

Slob, Wout .

CRITICAL REVIEWS IN TOXICOLOGY, 2007, 37 (05) :355-373

[5] Molecular identification of microsomal acyl-CoA:glycerol-3-phosphate acyltransferase, a key enzyme in de novo triacylglycerol synthesis [J].

Cao, Jingsong ;

Li, Jian-Liang ;

Li, Dongmei ;

Tobin, James F. ;

Gimeno, Ruth E. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (52) :19695-19700

[6] α-Terpineol induces fatty liver in mice mediated by the AMP-activated kinase and sterol response element binding protein pathway [J].

Choi, You-Jin ;

Sim, Woo-Cheol ;

Choi, Hyun Kyu ;

Lee, Seung-Ho ;

Lee, Byung-Hoon .

FOOD AND CHEMICAL TOXICOLOGY, 2013, 55 :129-136

[7]

Daniel GB, 1998, J NUCL MED, V39, P1286

[8] Metabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice [J].

Dumas, Marc-Emmanuel ;

Barton, Richard H. ;

Toye, Ayo ;

Cloarec, Olivier ;

Blancher, Christine ;

Rothwell, Alice ;

Fearnside, Jane ;

Tatoud, Roger ;

Blanc, Veronique ;

Lindon, John C. ;

Mitchell, Steve C. ;

Holmes, Elaine ;

McCarthy, Mark I. ;

Scott, James ;

Gauguier, Dominique ;

Nicholson, Jeremy K. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (33) :12511-12516

[9]

FOLCH J, 1957, J BIOL CHEM, V226, P497

[10]

Hawley Simon A, 2003, J Biol, V2, P28, DOI 10.1186/1475-4924-2-28

← 1 2 3 →