Physiology Unit, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain; Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Spain; Research in Neurobehavior and Health (NEUROLAB), Universitat Rovira i Virgili, Tarragona, Spain.
Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Spain; Research in Neurobehavior and Health (NEUROLAB), Universitat Rovira i Virgili, Tarragona, Spain; Biochemistry Unit, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain.
Food Chem Toxicol. 2020 Mar;137:111171. doi: 10.1016/j.fct.2020.111171. Epub 2020 Feb 1.
Chlorpyrifos (CPF) is an organophosphorus pesticide widely and extensively used in agriculture in more than one hundred countries and found ubiquitously in the environment. The present study was aimed at providing a better understanding of the obesogenic potential of CPF and its metabolites, as well as to evaluate their effects on the adipocyte differentiation process. For it, during the initial differentiation process, 3T3-L1 mouse preadipocytes were exposed to different concentrations of CPF, CPF-oxon (CPO), or 3,5,6-trichloropyridinol (TCP), which did not affect cell survival. Results showed how CPF and, to a lesser extent, its metabolite TCP, had a positive metabolic influence over the adipogenic process by fostering an increase in the number of differentiated 3T3-L1 preadipocytes, and by enhancing the capacity to store lipid droplets. These processes seem to occur through the upregulation of the transcription factors CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), which are related to a significant higher expression of the fatty acid-binding protein 4 (FABP4) adipokine. Based on this finding, CPF exposure could be one of the many factors that contributes to the worldwide increase in the incidence of obesity. However, additional investigations are clearly needed.
毒死蜱（CPF）是一种在一百多个国家广泛应用于农业的有机磷农药，在环境中普遍存在。本研究旨在更好地了解 CPF 及其代谢物的致肥胖潜力，并评估它们对脂肪细胞分化过程的影响。为此，在初始分化过程中，3T3-L1 小鼠前脂肪细胞暴露于不同浓度的 CPF、CPF-氧（CPO）或 3,5,6-三氯吡啶醇（TCP），这并没有影响细胞存活率。结果表明 CPF 及其代谢物 TCP 如何通过促进分化的 3T3-L1 前脂肪细胞数量的增加以及增强储存脂肪滴的能力，对脂肪生成过程产生积极的代谢影响。这些过程似乎是通过上调与脂肪酸结合蛋白 4（FABP4）脂肪因子的显著更高表达相关的转录因子 CCAAT/增强子结合蛋白α（C/EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ）来实现的。基于这一发现，CPF 暴露可能是导致全球肥胖发病率上升的众多因素之一。然而，显然还需要进一步的研究。
