3.8 Article

Dietary Regulation of Adult Stem Cells

期刊

CURRENT STEM CELL REPORTS
卷 3, 期 1, 页码 1-8

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s40778-017-0072-x

关键词

Diet; Mammalian adult stem cells

资金

  1. NCI NIH HHS [R01 CA211184, R01 CA034992] Funding Source: Medline
  2. NIA NIH HHS [R00 AG045144] Funding Source: Medline
  3. NIDDK NIH HHS [P30 DK043351] Funding Source: Medline
  4. NIGMS NIH HHS [T32 GM007287] Funding Source: Medline

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Purpose of Review Dietary intake is a critical regulator of organismal physiology and health. Tissue homeostasis and regeneration are dependent on adult tissue stem cells that self-renew and differentiate into the specialized cell types. As stem cells respond to cues from their environment, dietary signals and nutrients influence tissue biology by altering the function and activity of adult stem cells. In this review, we highlight recent studies that illustrate how diverse diets such as caloric restriction, fasting, high-fat diets, and ketogenic diets impact stem cell function and their microenvironments. Recent Findings Caloric restriction generally exerts positive effects on adult stem cells, notably increasing stem cell functionality in the intestine and skeletal muscle as well as increasing hematopoietic stem cell quiescence. Similarly, fasting confers protection of intestinal, hematopoietic, and neuronal stem cells against injury. High-fat diets induce intestinal stem cell niche independence and stem-like properties in intestinal progenitors, while high-fat diets impair hematopoiesis and neurogenesis. Summary Caloric restriction and fasting are generally beneficial to adult stem cell function, while high-fat diets impair stem cell function or create opportunities for tumorigenesis. However, the effects of each diet on stem cell biology are complex and vary greatly between tissues. Given the recent interest in developing dietary interventions or mimetics as therapeutics, further studies, including on ketogenic diets, will be essential to understand how adult stem cells respond to diet-induced signals and physiology.

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