Butyrate promotes C2C12 myoblast proliferation by activating ERK/MAPK pathway

• Published in: Molecular omics Vol. 19; no. 7; pp. 552 - 559
• Main Authors: Guan, Li, Cao, Ziyi, Pan, Ziyue, Zhao, Chao, Xue, Mengjuan, Yang, Fan, Chen, Jie
• Format: Journal Article
• Language: English
• Published: England 14.08.2023
• ISSN: 2515-4184; 2515-4184
• DOI: 10.1039/d2mo00256f

Sarcopenia has garnered considerable interest in recent years as ageing-associated diseases constitute a significant worldwide public health burden. Nutritional supplements have received much attention as potential tools for managing sarcopenia. However, the specific nutrients responsible are still under-investigated. In the current study, we first determined the levels of short chain fatty acids (SCFAs) and intestinal flora in the feces of elderly sarcopenia subjects and elderly healthy individuals by ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). Then cell viability detection, flow cytometry and transcriptome analysis were adopted to experimentally evaluate the effect and the underlying mechanism of SCFA on C2C12 cells proliferation in vitro . The results suggested that patients with sarcopenia exhibited decreased levels of butyrate. And butyrate may stimulate C2C12 myocyte proliferation via promoting G1/S cell cycle transition. Transcriptomic analyses pointed to upregulation of the Mitogen-activated protein kinase (MAPK) signaling pathway in butyrate-treated cells. In addition, the above proliferative phenotypes could be suppressed by the combination of ERK/MAPK inhibitor. A combined transcriptomic and metabolomic approach was applied in our study to investigate the potential effect of microbiota-derived butyrate yield on muscular proliferation which may indicate a protective effect of nutritional supplements. The role of butyrate, a metabolite of intestinal bacteria, in sarcopenia has received much attention in recent years.