Journal
NATURE COMMUNICATIONS
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms2668
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Funding
- Ministry of Education, Cultures, Sports, Science, and Technology
- Japan Science and Technology Agency
- National Center for Global Health and Medicine [21-110, 22-205, 21-129]
- Ministry of Health, Labor, and Welfare
- RIKEN RCAI
- Ministry of Health, Labor and Welfare of Japan
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Ministry of Agriculture, Forestry, and Fisheries of Japan
- Grants-in-Aid for Scientific Research [22689017, 24700455, 23590955, 24117524, 24658129, 24117723] Funding Source: KAKEN
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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.
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