Pulmonary exposure to diesel exhaust particles enhances fatty change of the liver in obese diabetic mice.
Pulmonary exposure to diesel exhaust particles enhances fatty change of the liver in obese diabetic mice.
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DOI：
10.3892/ijmm.19.1.17
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发表时间：
2007
影响因子：
5.4
通讯作者：
Makoto Tomaru;H. Takano;Ken-ichiro Inoue;R. Yanagisawa;N. Osakabe;A. Yasuda;A. Shimada;Y. Kato;H. Uematsu
中科院分区：
文献类型：
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作者：
Makoto Tomaru;H. Takano;Ken-ichiro Inoue;R. Yanagisawa;N. Osakabe;A. Yasuda;A. Shimada;Y. Kato;H. Uematsu
在流行病学研究中，暴露于环境颗粒物（PM）与糖尿病受试者的死亡率呈正相关。柴油机排气颗粒物（DEP）是大气PM的主要组成部分。然而，没有实验证据表明DEP与糖尿病及其并发症的关系。我们研究了DEP对糖尿病肥胖小鼠和对照小鼠的糖尿病变化和非酒精性脂肪性肝病（NAFLD）的影响。db/db小鼠和相应的非糖尿病db/+m小鼠每两周暴露于载体或DEP。用生化、组织学和免疫组织化学检查动物肝脏中的己酰赖氨酸（HEL）。在db/+m小鼠中，与溶剂相比，肺暴露于DEP不会增加天冬氨酸转氨酶（AST）或丙氨酸转氨酶（ALT）水平。然而，在db/db小鼠中，与溶剂相比，暴露于DEP会增加AST和ALT的水平。仅在db/db小鼠中，与溶剂相比，DEP增强了肝脏中脂肪变性的程度和HEL（氧化应激的标志物）的形成。这些结果表明，肺暴露于DEP、PM，可能通过增强的氧化应激增强肥胖糖尿病受试者肝脏中的脂肪变性。
In epidemiological studies, exposure to ambient particulate matter (PM) has been reported to be positively associated with mortality in subjects with diabetes mellitus. Diesel exhaust particles (DEP) are major constituents of atmospheric PM. However, there is no experimental evidence for the relation of DEP to diabetes mellitus and its complications. We investigated the effects of DEP inoculated intratracheally on diabetic changes and nonalcoholic fatty liver disease (NAFLD) in diabetic obese and control mice. db/db mice and the corresponding nondiabetic db/+m mice received exposure to vehicle or DEP every two weeks. Animals were examined with biochemistry, histology, and immunohistochemistry for hexanoyl-lysine (HEL) in the liver. In the db/+m mice, pulmonary exposure to DEP did not increase levels of aspartate aminotransferase (AST) or alanine aminotransferase (ALT) compared to that to vehicle. In the db/db mice, however, the exposure to DEP increased the levels of AST and ALT compared to that to vehicle. Only in the db/db mice, DEP enhanced the magnitude of steatosis and formation of HEL, a marker of oxidative stress, in the liver compared to vehicle. These results suggest that pulmonary exposure to DEP, PM, enhances steatosis in the liver of obese diabetic subjects possibly via enhanced oxidative stress.