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한빛사논문

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University of California at Davis

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Cell, February 15, 2024 | https://doi.org/10.1016/j.cell.2024.01.029 High fat intake sustains sorbitol intolerance after antibiotic-mediated Clostridia depletion from the gut microbiota

Jee-YonLee,¹ ConnorR.Tiffany,¹ ScottP.Mahan,¹ MatthewKellom,² AndrewW.L.Rogers,¹ HenryNguyen,¹ EricT.Stevens,³ HugoL.P.Masson,¹ KoheiYamazaki,^1,4 MariaL.Marco,³ EmileyA.Eloe-Fadrosh,² PeterJ.Turnbaugh,^5,6 and AndreasJ.Ba¨umler^1,7,*

¹Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave, Davis, CA95616, USA
²Environmental Genomics & Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, CA94720, USA ³Department of Food Science and Technology, University of California at Davis, Davis, CA95616, USA
⁴Laboratory of Veterinary Public Health, School of Veterinary Medicine, Kitasato University, Towada, Japan
⁵Department of Microbiology & Immunology, University of California, SanFrancisco, SanFrancisco, CA94143, USA
⁶Chan Zuckerberg Biohub-San Francisco, San Francisco, CA94158, USA
⁷Lead contact

^*Corresponding author: correspondence to AndreasJ.Ba¨umler

Abstract

Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.

논문정보

형식Research article
게재일2024년 02월 (BRIC 등록일 2024-02-19)
연구진국외 연구진
분야 생명과학 > 미생물학

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