State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, PR China.
Centre for Metabolism, Obesity and Diabetes Research, Canada; Division of Endocrinology and Metabolism, Department of Medicine, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Canada.
Curr Opin Pharmacol. 2022 Dec;67:102314. doi: 10.1016/j.coph.2022.102314. Epub 2022 Nov 2.
Rates of human obesity, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD) have risen faster than anticipated and cannot solely be explained by excessive caloric intake or physical inactivity. Importantly, this effect is also observed in many other domesticated and non-domesticated mammals, which has led to the hypothesis that synthetic environmental pollutants may be contributing to disease development. While the impact of these chemicals on appetite and adipogenesis has been extensively studied, their potential role in reducing energy expenditure is less studied. An important component of whole-body energy expenditure is adaptive and diet-induced thermogenesis in human brown adipose tissue (BAT). This review summarizes recent evidence that environmental pollutants such as the pesticide chlorpyrifos inhibit BAT function, diet-induced thermogenesis and the potential signaling pathways mediating these effects. Lastly, we discuss the importance of housing experimental mice at thermoneutrality, rather than room temperature, to maximize the translation of findings to humans.
肥胖症、2 型糖尿病和非酒精性脂肪性肝病 (NAFLD) 的发病率上升速度超出预期,不能仅仅用热量摄入过多或缺乏体力活动来解释。重要的是,这种现象在许多其他家养和非家养哺乳动物中也有观察到,这导致了一个假设,即合成环境污染物可能导致疾病的发生。虽然这些化学物质对食欲和脂肪生成的影响已经得到了广泛的研究,但它们在降低能量消耗方面的潜在作用研究得较少。全身能量消耗的一个重要组成部分是人类棕色脂肪组织 (BAT) 的适应性和饮食诱导的产热。这篇综述总结了最近的证据,表明像杀虫剂毒死蜱这样的环境污染物会抑制 BAT 功能、饮食诱导的产热以及介导这些作用的潜在信号通路。最后,我们讨论了将实验小鼠饲养在热中性温度(而非室温)下的重要性,以最大限度地将研究结果转化到人类身上。