期刊
NATURE
卷 600, 期 7890, 页码 713-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41586-021-04194-8
关键词
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资金
- EMBO Long Term Fellowship [2016-1088]
- European Union [747114]
- Leona M. and Harry B. Helmsley Charitable Trust
- Adelis Foundation
- Pearl Welinsky Merlo Scientific Progress Research Fund
- Park Avenue Charitable Fund
- Hanna and Dr. Ludwik Wallach Cancer Research Fund
- Daniel Morris Trust
- Wolfson Family Charitable Trust
- Wolfson Foundation
- Ben B. and Joyce E. Eisenberg Foundation
- White Rose International Foundation
- Estate of Malka Moskowitz
- Estate of Myron H. Ackerman
- Estate of Bernard Bishin for the WIS-Clalit Program
- Else Kroener Fresenius Foundation
- Jeanne and Joseph Nissim Center for Life Sciences Research
- Vainboim Family
- Swiss Society Institute for Cancer Prevention Research at the Weizmann Institute of Science, Rehovot, Israel
- European Research Council
- Israel Science Foundation
- Israel Ministry of Science and Technology
- Israel Ministry of Health
- Helmholtz Foundation
- Garvan Institute
- European Crohn's and Colitis Organization
- Deutsch-Israelische Projektkooperation
- IDSA Foundation
- Sagol Institute for Longevity Research Program
- Charlie Teo Foundation
- Wellcome Trust
- Marie Curie Actions (MSCA) [747114] Funding Source: Marie Curie Actions (MSCA)
Smoking and cessation induce a dysbiotic state in the intestines, leading to weight gain. Depletion of gut microbiota induced by antibiotics prevents weight gain after smoking cessation.
Cigarette smoking constitutes a leading global cause of morbidity and preventable death', and most active smokers report a desire or recent attempt to quite(2). Smoking-cessation-induced weight gain (SCWG; 4.5 kg reported to be gained on average per 6-12 months, >10 kg year(-1) in 13% of those who stopped smoking(3)) constitutes a major obstacle to smoking abstinence(4), even under stable' or restricted' caloric intake. Here we use a mouse model to demonstrate that smoking and cessation induce a dysbiotic state that is driven by an intestinal influx of cigarette-smoke-related metabolites. Microbiome depletion induced by treatment with antibiotics prevents SCWG. Conversely, fecal microbiome transplantation from mice previously exposed to cigarette smoke into germ-free mice naive to smoke exposure induces excessive weight gain across diets and mouse strains. Metabolically, microbiome-induced SCWG involves a concerted host and microbiome shunting of dietary choline to dimethylglycine driving increased gut energy harvest, coupled with the depletion of a cross-regulated weight-lowering metabolite, N-acetylglycine, and possibly by the effects of other differentially abundant cigarette-smoke-related metabolites. Dimethylglycine and N-acetylglycine may also modulate weight and associated adipose-tissue immunity under non-smoking conditions. Preliminary observations in a small cross-sectional human cohort support these findings, which calls for larger human trialsto establish the relevance of this mechanism in active smokers. Collectively, we uncover a microbiome-dependent orchestration of SCWG that may be exploitable to improve smoking-cessation success and to correct metabolic perturbations even in non-smoking settings.
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