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1,3-二氯-2-丙醇通过 AMPK 信号通路诱导 C57BL/6J 小鼠发生高血脂症。

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

机构信息

Department of Food Quality and Safety, Jilin University, Changchun, People's Republic of China.

Department of Food Quality and Safety, Jilin University, Changchun, People's Republic of China.

出版信息

Food Chem Toxicol. 2014 Feb;64:403-9. doi: 10.1016/j.fct.2013.11.049. Epub 2013 Dec 11.

DOI:10.1016/j.fct.2013.11.049
PMID:24333398
Abstract

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, 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.

摘要

1,3-二氯-2-丙醇(1,3-DCP)是一种广泛存在于各种食品中的已知污染物。膳食摄入是接触 1,3-DCP 的最大来源。在这项研究中,我们首先发现 1,3-DCP 可以在低于 1mg/kg/天的剂量下诱导 C57BL/6J 小鼠发生高血脂症。我们研究了血清脂质谱、肝总胆固醇(TC)和甘油三酯(TG)、肝和脂肪组织的组织病理学。结果表明,1,3-DCP 呈剂量依赖性地增加血清 TG、TC 和低密度脂蛋白胆固醇(LDL-C),降低血清高密度脂蛋白胆固醇(HDL-C),增加相对肝重、肝 TG 和 TC、相对脂肪组织重量,并使脂肪细胞增大。由于 AMPK 信号通路在脂质代谢过程中非常重要,我们进一步研究了 1,3-DCP 对小鼠模型中 AMPK 信号通路的影响。结果表明,1,3-DCP(0.1-1mg/kg/天)降低了 p-AMPK/tAMPK 比值、p-ACC/tACC 比值、PPARα 的表达,但增加了 FAT、SREBP1、HMGCR 和 FAS 的表达。这些观察结果表明,1,3-DCP 通过调节 AMPK 信号通路至少部分导致 C57BL/6J 小鼠发生高血脂症。

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