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, Taeko Dohi

研究成果: Article査読

88 被引用数 (Scopus)


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.

ジャーナルNature communications
出版ステータスPublished - 2013

ASJC Scopus subject areas

  • 化学 (全般)
  • 生化学、遺伝学、分子生物学(全般)
  • 物理学および天文学(全般)


「Microbiota-derived lactate accelerates colon epithelial cell turnover in starvation-refed mice」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。