High fat diet activates adult mouse lung stem cells and accelerates several aging-induced effects

Ahmed E. Hegab, Mari Ozaki, Fatma Y. Meligy, Shizuko Kagawa, Makoto Ishii, Tomoko Betsuyaku

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


High fat diet (HFD) decreases the lifespan of mice, and is a risk factor for several human diseases. Here, we investigated the effects of a HFD on lung epithelial and stem cells and its interaction with aging. Young and old mice were fed with either a standard diet (SD) or a HFD then their trachea and lung were examined for histological changes, inflammation, and mitochondrial function. Their stem cell function was examined using the in vitro organoid/colony forming efficiency (CFE) assay. Aging reduced the number of tracheal basal and alveolar type-2 (AT2) cells. HFD significantly increased the number of AT2 cells. Aging also caused a significant increase in lung inflammation, and HFD caused a similar increase, in young mice. Aging reduced mitochondrial mass and function, and increased reactive oxygen species. In young mice, HFD caused mitochondrial changes similar to the aging-induced changes. Organoid culture of tracheal and lung epithelial cells collected from both young and old HFD-fed mice showed higher CFE compared to SD-fed mice. Switching the HFD to low calorie/fat diet (LCD) efficiently reversed several of the HFD-induced effects. Thus, HFD induces several histological, inflammatory, and functional changes in the lung, and exacerbates the aging-induced lung inflammation and mitochondrial deterioration. LCD can reverse many of the HFD-induced effects.

Original languageEnglish
Pages (from-to)25-35
Number of pages11
JournalStem Cell Research
Publication statusPublished - 2018 Dec


  • Aging
  • Alveolar cells
  • Calorie restriction
  • High fat diet
  • Lung stem cells
  • Mitochondria

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology


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