Lactational delivery of Triclosan promotes non-alcoholic fatty liver disease in newborn mice

André A. Weber, Xiaojing Yang, Elvira Mennillo, Jeffrey Ding, Jeramie D. Watrous, Mohit Jain, Shujuan Chen, Michael Karin and Robert H. Tukey ()
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André A. Weber: University of California, San Diego
Xiaojing Yang: University of California, San Diego
Elvira Mennillo: University of California, San Diego
Jeffrey Ding: University of California, San Diego
Jeramie D. Watrous: University of California, San Diego
Mohit Jain: University of California, San Diego
Shujuan Chen: University of California, San Diego
Michael Karin: University of California, San Diego
Robert H. Tukey: University of California, San Diego

Nature Communications, 2022, vol. 13, issue 1, 1-13

Abstract: Abstract Here we show that Triclosan (TCS), a high-volume antimicrobial additive that has been detected in human breastmilk, can be efficiently transferred by lactation to newborn mice, causing significant fatty liver (FL) during the suckling period. These findings are relevant since pediatric non-alcoholic fatty liver disease (NAFLD) is escalating in the United States, with a limited mechanistic understanding. Lactational delivery stimulated hepatosteatosis, triglyceride accumulation, endoplasmic reticulum (ER) stress, signs of inflammation, and liver fibrosis. De novo lipogenesis (DNL) induced by lactational TCS exposure is shown to be mediated in a PERK-eIF2α-ATF4-PPARα cascade. The administration of obeticholic acid (OCA), a potent FXR agonist, as well as activation of intestinal mucosal-regenerative gp130 signaling, led to reduced liver ATF4 expression, PPARα signaling, and DNL when neonates were exposed to TCS. It is yet to be investigated but mother to child transmission of TCS or similar toxicants may underlie the recent increases in pediatric NAFLD.

Date: 2022
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DOI: 10.1038/s41467-022-31947-4

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