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The pesticide chlorpyrifos promotes obesity by inhibiting diet-induced thermogenesis in brown adipose tissue. 2021
Bo Wang, and
Evangelia E Tsakiridis, and
Shuman Zhang, and
Andrea Llanos, and
Eric M Desjardins, and
Julian M Yabut, and
Alexander E Green, and
Emily A Day, and
Brennan K Smith, and
James S V Lally, and
Jianhan Wu, and
Amogelang R Raphenya, and
Krishna A Srinivasan, and
Andrew G McArthur, and
Shingo Kajimura, and
Jagdish Suresh Patel, and
Michael G Wade, and
Katherine M Morrison, and
Alison C Holloway, and
Gregory R Steinberg
Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, ON, Canada.
Obesity results from a caloric imbalance between energy intake, absorption and expenditure. In both rodents and humans, diet-induced thermogenesis contributes to energy expenditure and involves the activation of brown adipose tissue (BAT). We hypothesize that environmental toxicants commonly used as food additives or pesticides might reduce BAT thermogenesis through suppression of uncoupling protein 1 (UCP1) and this may contribute to the development of obesity. Using a step-wise screening approach, we discover that the organophosphate insecticide chlorpyrifos suppresses UCP1 and mitochondrial respiration in BAT at concentrations as low as 1 pM. In mice housed at thermoneutrality and fed a high-fat diet, chlorpyrifos impairs BAT mitochondrial function and diet-induced thermogenesis, promoting greater obesity, non-alcoholic fatty liver disease (NAFLD) and insulin resistance. This is associated with reductions in cAMP; activation of p38MAPK and AMPK; protein kinases critical for maintaining UCP1 and mitophagy, respectively in BAT. These data indicate that the commonly used pesticide chlorpyrifos, suppresses diet-induced thermogenesis and the activation of BAT, suggesting its use may contribute to the obesity epidemic.
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