Microbiota-derived lactate accelerates colon epithelial cell turnover in starvation-refed mice

Toshihiko Okada, Shinji Fukuda, Koji Hase, Shin Nishiumi, Yoshihiro Izumi, Masaru Yoshida, Teruki Hagiwara, Rei Kawashima, Motomi Yamazaki, Tomoyuki Oshio, Takeshi Otsubo, Kyoko Inagaki-Ohara, Kazuki Kakimoto, Kazuhide Higuchi, Yuki I. Kawamura, Hiroshi Ohno and Taeko Dohi ()
Additional contact information
Toshihiko Okada: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Shinji Fukuda: Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology
Koji Hase: Graduate School of Nanobioscience, Yokohama City University
Shin Nishiumi: Kobe University Graduate School of Medicine
Yoshihiro Izumi: Kobe University Graduate School of Medicine
Masaru Yoshida: Kobe University Graduate School of Medicine
Teruki Hagiwara: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Rei Kawashima: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Motomi Yamazaki: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Tomoyuki Oshio: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Takeshi Otsubo: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Kyoko Inagaki-Ohara: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Kazuki Kakimoto: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Kazuhide Higuchi: Osaka Medical College
Yuki I. Kawamura: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine
Hiroshi Ohno: Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology
Taeko Dohi: Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: Abstract Oral food intake influences the morphology and function of intestinal epithelial cells and maintains gastrointestinal cell turnover. However, how exactly these processes are regulated, particularly in the large intestine, remains unclear. Here we identify microbiota-derived lactate as a major factor inducing enterocyte hyperproliferation in starvation-refed mice. Using bromodeoxyuridine staining, we show that colonic epithelial cell turnover arrests during a 12- to 36-h period of starvation and increases 12–24 h after refeeding. Enhanced epithelial cell proliferation depends on the increase in live Lactobacillus murinus, lactate production and dietary fibre content. In the model of colon tumorigenesis, mice exposed to a carcinogen during refeeding develop more aberrant crypt foci than mice fed ad libitum. Furthermore, starvation after carcinogen exposure greatly reduced the incidence of aberrant crypt foci. Our results indicate that the content of food used for refeeding as well as the timing of carcinogen exposure influence the incidence of colon tumorigenesis in mice.

Date: 2013
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DOI: 10.1038/ncomms2668

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