Metformin-induced metabolic reprogramming inhibits the proliferation and differentiation of myoblasts
10.16289/j.cnki.1002-0837.2025.03004
- VernacularTitle:二甲双胍诱导代谢重编程抑制成肌细胞的增殖分化
- Author:
Rongxi PU
1
;
Fan BU
;
Siyuan HUANG
;
Zhong YANG
Author Information
1. 陆军军医大学药学与检验医学系,重庆 400038
- Keywords:
myoblasts;
energy metabolism;
metformin;
AMP-activated protein kinase;
proliferation;
differentiation
- From:Space Medicine & Medical Engineering
2025;36(3):214-219
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects and mechanisms of metformin-induced metabolic intervention on the proliferation and differentiation of myoblasts.Methods C2C12 myoblasts cultured in growth or differentiation media were treated with 1 mmol/L metformin,with DMSO as the control.Cells in growth media were treated for 48 hours,with samples collected every 12 hours for metabolomic analysis,protein expression,mitochondrial function,and proliferation assays.Cells in differentiation media were induced to differentiate for 72 hours,and myotube formation was assessed via embryonic myosin heavy chain immunofluorescence staining.Results Metformin treatment increased intracellular levels of metabolites such as lactate,pyruvate,and adenosine monophosphate,while reducing adenosine triphosphate and thiamine pyrophosphate.Phosphorylation of AMP-activated protein kinase(AMPK)and related protein expression were significantly upregulated(P<0.05).Mitochondrial biogenesis was enhanced,and membrane potential markedly decreased(P<0.05).The proportion of S-phase cells and EdU-positive cells gradually increased(P<0.01),though overall proliferation rate slowed.During differentiation,the myoblast fusion index significantly decreased(P<0.01).Conclusion Metformin induces metabolic reprogramming in myoblasts and suppresses their proliferation and differentiation,with activation of AMPK-related signaling pathways serving as a key molecular mechanism.
