Metformin attenuates an increase of calcium-dependent and ubiquitin-proteasome markers in unloaded muscle
С. П. Белова, Ksenia A. Zaripova, Kristina A. Sharlo, Tatiana Y. Kostrominova, Boris Shenkman, T. L. Nemirovskaya
Abstract
Current study for the first time tested the hypothesis that during 3 days of soleus muscle unloading, calcium-dependent signaling pathways, markers of protein synthesis, and the expression of E3 ubiquitin ligases can be regulated by metformin. Treatment with metformin during unloading: prevented the decrease of p-AMPK and increase of ATP content, affected regulation of calcium-dependent signaling pathways, and attenuated an increase of critical markers of ubiquitin-proteasome pathways. Nevertheless, metformin treatment has not prevented soleus muscle atrophy.
Topics & Concepts
Soleus muscleAMPKEndocrinologyInternal medicineCalpainMetforminDownregulation and upregulationUbiquitinAMP-activated protein kinasePhosphorylationProtein kinase ASkeletal muscleAutophagyChemistryBiologyCell biologyBiochemistryEnzymeMedicineApoptosisInsulinGeneMuscle Physiology and DisordersAutophagy in Disease and TherapyAdipose Tissue and Metabolism