作者
Bo Chen,Lulu Sun,Guangyi Zeng,Zhe Shen,Kai Wang,Limin Yin,Feng Xu,Pengcheng Wang,Yong Ding,Qixing Nie,Qing Wu,Zhiwei Zhang,Jialin Xia,Jun Lin,Yuhong Luo,Jie Cai,Kristopher W. Krausz,Ruimao Zheng,Yan-Xue Xue,Ming‐Hua Zheng,Yang Li,Chaohui Yu,Frank J. Gonzalez,Changtao Jiang
摘要
Tobacco smoking is positively correlated with non-alcoholic fatty liver disease (NAFLD)1–5, but the underlying mechanism for this association is unclear. Here we report that nicotine accumulates in the intestine during tobacco smoking and activates intestinal AMPKα. We identify the gut bacterium Bacteroides xylanisolvens as an effective nicotine degrader. Colonization of B. xylanisolvens reduces intestinal nicotine concentrations in nicotine-exposed mice, and it improves nicotine-exacerbated NAFLD progression. Mechanistically, AMPKα promotes the phosphorylation of sphingomyelin phosphodiesterase 3 (SMPD3), stabilizing the latter and therefore increasing intestinal ceramide formation, which contributes to NAFLD progression to non-alcoholic steatohepatitis (NASH). Our results establish a role for intestinal nicotine accumulation in NAFLD progression and reveal an endogenous bacterium in the human intestine with the ability to metabolize nicotine. These findings suggest a possible route to reduce tobacco smoking-exacerbated NAFLD progression. Nicotine accumulates in the intestine during tobacco smoking and accelerates the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis (NASH), but it can be degraded effectively by the human symbiont Bacteroides xylanisolvens.