Barthez Marine, Song Zehan, Wang Chih Ling, Chen Danica
Program in Metabolic Biology, Nutritional Sciences & Toxicology, University of California, Berkeley, CA 94720.
Program in Metabolic Biology, Nutritional Sciences & Toxicology, University of California, Berkeley, CA 94720, 119 Morgan Hall, University of California, Berkeley, CA 94720.
Curr Stem Cell Rep. 2020 Dec;6(4):119-125. doi: 10.1007/s40778-020-00180-4. Epub 2020 Oct 28.
Diet has profound impacts on health and longevity. Evidence is emerging to suggest that diet impinges upon the metabolic pathways in tissue-specific stem cells to influence health and disease. Here, we review the similarities and differences in the metabolism of stem cells from several tissues, and highlight the mitochondrial metabolic checkpoint in stem cell maintenance and aging. We discuss how diet engages the nutrient sensing metabolic pathways and impacts stem cell maintenance. Finally, we explore the therapeutic implications of dietary and metabolic regulation of stem cells.
Stem Cell transition from quiescence to proliferation is associated with a metabolic switch from glycolysis to mitochondrial OXPHOS and the mitochondrial metabolic checkpoint is critically controlled by the nutrient sensors SIRT2, SIRT3, and SIRT7 in hematopoietic stem cells. Intestine stem cell homeostasis during aging and in response to diet is critically dependent on fatty acid metabolism and ketone bodies and is influenced by the niche mediated by the nutrient sensor mTOR.
Nutrient sensing metabolic pathways critically regulate stem cell maintenance during aging and in response to diet. Elucidating the molecular mechanisms underlying dietary and metabolic regulation of stem cells provides novel insights for stem cell biology and may be targeted therapeutically to reverse stem cell aging and tissue degeneration.
饮食对健康和寿命有着深远影响。越来越多的证据表明，饮食会影响组织特异性干细胞中的代谢途径，进而影响健康与疾病。在此，我们综述了几种组织中干细胞代谢的异同，并强调了干细胞维持和衰老过程中的线粒体代谢检查点。我们讨论了饮食如何参与营养感应代谢途径并影响干细胞维持。最后，我们探讨了干细胞饮食和代谢调节的治疗意义。
干细胞从静止状态转变为增殖状态与从糖酵解到线粒体氧化磷酸化的代谢转换相关，造血干细胞中的线粒体代谢检查点由营养传感器SIRT2、SIRT3和SIRT7严格控制。衰老过程中以及对饮食作出反应时，肠道干细胞的稳态严重依赖脂肪酸代谢和酮体，并受到营养传感器mTOR介导的微环境的影响。
营养感应代谢途径在衰老过程中以及对饮食作出反应时严格调节干细胞维持。阐明干细胞饮食和代谢调节的分子机制为干细胞生物学提供了新的见解，并且可能成为逆转干细胞衰老和组织退化的治疗靶点。
