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典型持久性有机污染物参与糖尿病发生的机制研究进展

Research progress on mechanisms of typical persistent organic pollutants involved in development of diabetes mellitus
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摘要 环境污染一直被认为是糖尿病发生的诱因之一,近年来众多研究表明环境持久性有机污染物(POPs)可能与糖尿病发生发展密切相关。本文依据POPs常规分类,以有机氯农药对双氯苯基双氯乙烷(DDT)、工业化学品多氯联苯(PCB)以及工业副产物四氯二苯并-p-二噁英(TCDD)为典型代表,归纳了其在糖尿病发病过程中的最新分子机制,指出除氧化应激作为各类POPs诱发糖尿病的普遍通路外,PCB、TCDD等对炎症反应以及胰腺发育缺陷等主要环节中相关靶点如肝细胞核因子1b(HNF1b)、细胞色素氧化酶P450 1A1(CYP1A1)以及相关基因DNA甲基化模式的调控成为新的研究方向,为进一步开展对POPs与糖尿病相关发病机制研究及糖尿病的防治提供科学依据。 Environmental pollution has always been considered as one of the causes of diabetes. In recent years, many studies have shown that environmental persistent organic pollutants(POPs) may be closely related to the occurrence and development of diabetes. According to conventional classification of POPs, taking organochlorine pesticides(dichlorodiphenyltrichloroe thane, DDT), industrial chemicals(polychlorinated biphenyl, PCB), and industrial by-products(tetrachlorodibenzo-p-dioxin, TCDD) as representatives, this paper summarized the latest molecular mechanisms in the pathogenesis of diabetes, and pointed out that in addition to oxidative stress as a common pathway for various POPs to induce diabetes, the regulations of PCB and TCDD to other related targets such as hepatocyte nuclear factor 1b(HNF1b), cytochrome P450 1A1(CYP1A1) in major links of inflammatory response and pancreatic developmental defects and the DNA methylation patterns of related genes have become new research directions. The paper aimed to provide a scientific basis for further research on POPs in association with pathogenesis of diabetes, and the prevention and treatment of diabetes.
作者 郭晓晨 高明 吴南翔 GUO Xiaochen;GAO Ming;WU Nanxiang(Hangzhou Medical College,Hangzhou,Zhejiang 310053,China;Zhejiang Academy of Medical Science,Hangzhou,Zhejiang 310013,China)
出处 《环境与职业医学》 CAS CSCD 北大核心 2021年第5期553-557,共5页 Journal of Environmental and Occupational Medicine
基金 浙江省自然科学基金(LQ20H260001)。
关键词 持久性有机污染物 糖尿病 分子机制 糖脂代谢 胰岛功能 persistent organic pollutant diabetes mellitus molecular mechanism glucose and lipid metabolism islet function
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