"Novel functions of vitamin B6 beyond its general known nutritional value in regulating muscle satellite cells" reported by Thanutchaporn Kumrungsee

Key points of this research

  • This study is the first to demonstrate the role of vitamin B6 in satellite cell function and its potential application in sarcopenia prevention.
  • Vitamin B6 deficiency appears to induce a decline in the quiescent satellite cell pool.
  • Vitamin B6 is essential for maintaining the proliferation and self-renewal of satellite cells during myogenesis.

Content of research

Satellite cells are muscle stem cells playing an important role in muscle regeneration. In aging people, numbers and function of satellite cells gradually decrease, leading to a reduction in muscle regeneration ability consequent to a loss of muscle mass and function, termed sarcopenia. Therefore, if we can preserve the number and function of satellite cells in aging muscles, we can possibly prevent or retard sarcopenia. Currently, there is no drug to treat sarcopenia. The lonely available recommendations for sarcopenia management are exercise and nutrition, in which the most extensively studied nutrients are proteins, amino acids, vitamin D, and omega 3 fatty acids. However, recent studies, during 2016-2021, suggest that older people in European countries and Japan who have sarcopenia often have low intake and low blood levels of vitamin B6. These emerging research results led us to hypothesize that vitamin B6 deficiency may be involved in the development of sarcopenia through impacting satellite cells.

【Research content】
In the present study, we determined if vitamin B6 deficiency exhibits any adverse effects on the number and function of satellite cells. We applied a single muscle fiber technique that allowed us to observe the number and function of the satellite cells, while they remained in their niche on the muscle fibers, thereby ensuring that the conditions resemble the normal physiological state. We isolated single muscle fibers from the skeletal muscles of mice fed a low vitamin B6 diet (deficiency) and a high vitamin B6 diet (supplementation). Then, the muscle fibers were cultured for 0, 24, 48, and 72 h, followed by observing changes in the number and function of the satellite cells on those muscle fibers under a fluorescent microscope as shown in the representative images in figure 1A-C. Under normal conditions, the satellite cells are in a quiescent or inactive state, stained positive with Pax7, (Figure 1A). Upon activation due to injury or diseases, quiescent satellite cells enter the cell cycle and proliferate to produce a large number of satellite cell progenies, stained positive with Pax7 and MyoD, as shown in Figure 1B and C. When time passes, these cells further undergo differentiation and fusion with the damaged muscle fibers giving rise to regenerating muscle fibers, or undergo self-renewal that helps to return the satellite cells to their quiescent state to replenish the satellite cell pool as shown in Figure 1D. As a result, we found that the muscle fibers isolated from mice fed the low vitamin B6 diet exhibited a significant lower number of quiescent, proliferating, and self-renewing satellite cells. The vitamin B6-free medium further worsen these adverse effects. In summary, it seems likely that vitamin B6 deficiency reduces the number of quiescent satellite cells and inhibits the proliferation and self-renewal of satellite cells during myogenesis. 

【Future development】
In our future works, we will further elucidate the mechanisms of how vitamin B6 regulates the proliferation and self-renewal of satellite cells. The role of vitamin B6 in muscle regeneration and muscle atrophy will be clarified. We believe that these findings will lead to the development of nutritional interventions for sarcopenia treatment in the future.

Information details of publication

  • Journal: Nutrients
  • Title: Satellite Cells Exhibit Decreased Numbers and Impaired Functions on Single Myofibers Isolated from Vitamin B6-Deficient Mice
  • Authors: Takumi Komaru, Noriyuki Yanaka, and Thanutchaporn Kumrungsee
  • DOI: https://doi.org/10.3390/nu13124531

Associate Professor Thanutchaporn Kumrungsee
School of Applied Biological Science, Hiroshima University
Tel:082-424-7980 FAX:082-424-2459
E-mail:kumrung*hiroshima-u.ac.jp (Note: Please replace *with @)