The First Affiliated Hospital (School of Clinical Medicine), Guangdong Pharmaceutical University, Nong-Lin-Xia Road 19(#), Yue-Xiu District, Guangzhou, 510080, PR China.
Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, 510006, PR China; School of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, 510006, PR China.
Toxicology. 2021 Feb 28;450:152678. doi: 10.1016/j.tox.2021.152678. Epub 2021 Jan 10.
Exposure of humans to second-hand smoking (SHS) increases glucose and lipid metabolic disorders. The link of hepatic metabolic dysfunction to environmental cigarette smoking has been noticed, but the related mechanism is still unclear. C57BL/6 mice with normal food diet (NFD) or high fat diet (HFD) were exposed to 15 min cigarette smoking twice a day in a 0.038 m box for 4 weeks, and the concentration of nicotine in the air of the box was 21.05 mg/m during the smoke exposure. Liver tissues and serum were collected for gene expression and biochemistry test. The fecal microbiota was also checked through 16S rDNA sequences. Cigarette smoking exposure increased the accumulation of total cholesterol (TC) in liver, and the expression of cholesterol synthesis-related genes was upregulated. The expression of CYP8B1 protein was significantly down-regulated, and the ratio of cholic acid (CA) to chenodeoxycholic acid (CDCA) was significantly reduced in the liver of mice exposed to cigarette smoking especially for HFD group. Cigarette smoking exposure caused insulin resistance in the liver of mice with HFD. The composition of the gut microbiota was altered with the exposure of cigarette smoking, and the change of the distribution of primary bile acids might be one of the reasons. It was concluded that cigarette smoking would break the homeostasis of cholesterol and bile acids metabolism and changed the composition of gut microbiota. Our discoveries confirmed that smoking bans are important for the public health.
人体暴露于二手烟（SHS）会增加葡萄糖和脂质代谢紊乱。已经注意到肝代谢功能障碍与环境香烟烟雾之间存在联系，但相关机制尚不清楚。将正常饮食（NFD）或高脂肪饮食（HFD）的 C57BL/6 小鼠暴露于 0.038 m 箱中的香烟烟雾中，每天两次，每次 15 分钟，持续 4 周，箱内空气中的尼古丁浓度为 21.05 mg/m。收集肝组织和血清进行基因表达和生化测试。还通过 16S rDNA 序列检查粪便微生物群。吸烟暴露会增加肝脏总胆固醇（TC）的积累，并上调胆固醇合成相关基因的表达。CYP8B1 蛋白的表达显著下调，尤其是在暴露于香烟烟雾的 HFD 组小鼠的肝脏中，胆酸（CA）与鹅脱氧胆酸（CDCA）的比值显著降低。吸烟暴露会导致 HFD 小鼠肝脏胰岛素抵抗。吸烟暴露会改变肠道微生物群的组成，初级胆汁酸的分布变化可能是原因之一。结论是，吸烟会破坏胆固醇和胆汁酸代谢的内稳态，并改变肠道微生物群的组成。我们的发现证实了禁烟对公众健康的重要性。
