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农药暴露对脂肪组织发育和功能的影响。

Impact of pesticide exposure on adipose tissue development and function.

机构信息

Centre for Metabolism, Obesity and Diabetes Research, McMaster University, 1280 Main St. W., Hamilton, ON, Canada L8N 3Z5.

Department of Obstetrics and Gynecology, McMaster University, 1280 Main St. W., Hamilton, ON, Canada L8N 3Z5.

出版信息

Biochem J. 2020 Jul 31;477(14):2639-2653. doi: 10.1042/BCJ20200324.

Abstract

Obesity is a leading cause of morbidity, mortality and health care expenditure whose incidence is rapidly rising across the globe. Although the cause of the obesity epidemic is typically viewed as a product of an increased availability of high calorie foods and/or a reduction in physical activity, there is mounting evidence that exposure to synthetic chemicals in our environment may play an important role. Pesticides, are a class of chemicals whose widespread use has coincided with the global rise of obesity over the past two decades. Importantly, given their lipophilic nature many pesticides have been shown to accumulate with adipose tissue depots, suggesting they may be disrupting the function of white adipose tissue (WAT), brown adipose tissue (BAT) and beige adipose tissue to promote obesity and metabolic diseases such as type 2 diabetes. In this review, we discuss epidemiological evidence linking pesticide exposure with body mass index (BMI) and the incidence of diabetes. We then review preclinical studies in rodent models which have directly evaluated the effects of different classes of insecticides and herbicides on obesity and metabolic dysfunction. Lastly, we review studies conducted in adipose tissue cells lines and the purported mechanisms by which pesticides may induce alterations in adipose tissue function. The review of the literature reveals major gaps in our knowledge regarding human exposure to pesticides and our understanding of whether physiologically relevant concentrations promote obesity and elicit alterations in key signaling pathways vital for maintaining adipose tissue metabolism.

摘要

肥胖是发病率、死亡率和医疗支出的主要原因,其发病率在全球范围内迅速上升。尽管肥胖症的病因通常被认为是高热量食物供应增加和/或体力活动减少的结果,但越来越多的证据表明,我们环境中接触的合成化学物质可能发挥着重要作用。农药是一类化学物质,其广泛使用恰逢过去二十年来肥胖在全球范围内的上升。重要的是,鉴于它们的亲脂性,许多农药已被证明会在脂肪组织库中积累,这表明它们可能会破坏白色脂肪组织 (WAT)、棕色脂肪组织 (BAT) 和米色脂肪组织的功能,从而促进肥胖和代谢疾病,如 2 型糖尿病。在这篇综述中,我们讨论了将农药暴露与体重指数 (BMI) 和糖尿病发病率联系起来的流行病学证据。然后,我们回顾了在啮齿动物模型中进行的直接评估不同类别的杀虫剂和除草剂对肥胖和代谢功能障碍影响的临床前研究。最后,我们回顾了在脂肪组织细胞系中进行的研究以及关于农药可能通过何种机制引起脂肪组织功能改变的假设机制。对文献的回顾揭示了我们在人类暴露于农药方面的知识存在重大差距,以及我们是否理解生理相关浓度是否会促进肥胖并引发维持脂肪组织代谢的关键信号通路的改变。

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