Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review.

Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review.
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DOI:
10.1289/ehp.1104597
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发表时间:
2012-06
影响因子:
10.4
通讯作者:
Gallo MA
Gallo MA
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Thayer KA;Heindel JJ;Bucher JR;Gallo MA

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背景:人们越来越关注环境化学物质的暴露可能是糖尿病和肥胖症流行的因素这一概念。 2011 年 1 月 11 日至 13 日,国家毒理学计划 (NTP) 的国家环境健康科学研究所 (NIEHS) 部门组织了一次研讨会,以评估这些日益引起公众健康关注的主题的科学现状。目的:研讨会的主要目的是在完成对暴露于某些环境化学品的人类和实验动物的文献的批判性分析后,为研究议程制定建议。研讨会考虑的环境暴露包括砷、持久性有机污染物、孕产妇吸烟/尼古丁、有机锡、邻苯二甲酸盐、双酚A和农药。 21 世纪毒理学 (Tox21) 的高通量筛选数据也被认为是评估潜在细胞途径并生成假设的一种方法,用于测试哪些化学物质以及如何干扰与糖尿病和肥胖相关的生物过程。结论:总体而言,对现有文献的回顾确定了几种环境暴露与 2 型糖尿病之间的联系。 “发育性肥胖”假说也得到了支持,该假说表明,化学物质暴露可能会通过改变脂肪细胞的分化或调节进食行为的神经回路的发育来增加肥胖的风险。当发育暴露与​​晚年摄入高热量、高碳水化合物或高脂肪饮食相结合时,这种影响可能最为明显。关于环境化学物质暴露和 1 型糖尿病的研究非常有限。研究的缺乏被认为是一个关键的数据差距。在本次研讨会回顾中,我们概述了研讨会中出现的主要主题,并讨论了 NIEHS/NTP 为解决研究建议而开展的活动。这篇评论还作为即将发布的一系列文章的介绍,这些文章更详细地回顾了有关特定暴露和结果的文献。
Background: There has been increasing interest in the concept that exposures to environmental chemicals may be contributing factors to the epidemics of diabetes and obesity. On 11–13 January 2011, the National Institute of Environmental Health Sciences (NIEHS) Division of the National Toxicology Program (NTP) organized a workshop to evaluate the current state of the science on these topics of increasing public health concern. Objective: The main objective of the workshop was to develop recommendations for a research agenda after completing a critical analysis of the literature for humans and experimental animals exposed to certain environmental chemicals. The environmental exposures considered at the workshop were arsenic, persistent organic pollutants, maternal smoking/nicotine, organotins, phthalates, bisphenol A, and pesticides. High-throughput screening data from Toxicology in the 21st Century (Tox21) were also considered as a way to evaluate potential cellular pathways and generate -hypotheses for testing which and how certain chemicals might perturb biological processes related to diabetes and obesity. Conclusions: Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life. Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap. In this workshop review, we outline the major themes that emerged from the workshop and discuss activities that NIEHS/NTP is undertaking to address research recommendations. This review also serves as an introduction to an upcoming series of articles that review the literature regarding specific exposures and outcomes in more detail.
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