Microbiota-derived lactate and dietary responses of colonocytes; molecular bases for the manipulation of cell turnover by changing eating behavior to avoid cancer risk

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04503
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Food science
• Research Institution: National Center for Global Health and Medicine
• Principal Investigator: Dohi Taeko 国立研究開発法人国立国際医療研究センター, 消化器疾患研究部, 部長 (60250221)
• Research Collaborator: KAWAMURA Yuki I 国立国際医療研究センター研究所, 肝炎・免疫研究センター消化器疾患研究部, 室長
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 絶食 / 乳酸 / 大腸 / 肥満

Outline of Final Research Achievements

Turnover of gastrointestinal epithelial cells arrests at fasting, while refeeding induces transient hyperproliferation by the action of lumenal lactate produced by commensal microbiota. In this study, we found that this physiological response of colonocytes to fasting-refeeding was disturbed in high fat diet-fed obese mice, which resulted in the increased risk of carcinogenesis. However, we also showed that manipulation of colonocyte turnover with delivery of lactate into the colon lumen and setting appropriate fasting period was able to reduce colonic inflammation, promote epithelial repair, and reduce the risk of carcinogenesis.

Free Research Field

消化器病学