scholarly journals Changes in intracellular ion activities induced by adrenaline in human and rat skeletal muscle

1988 ◽  
Vol 411 (3) ◽  
pp. 283-288 ◽  
Author(s):  
Klaus Ballanyi ◽  
Peter Grafe
Keyword(s):  
Skeletal Muscle ◽  
Rat Skeletal Muscle ◽  
Intracellular Ion Activities ◽  
Ion Activities

In vitro studies on the effect of glucocorticoids on the metabolism of perfused rat skeletal muscle

1984 ◽  
Vol 104 (4_Supplb) ◽  
pp. S110-S111
Author(s):  
P. SCHADEWALDT ◽  
H. MEYER
Keyword(s):  
Skeletal Muscle ◽  
In Vitro Studies ◽  
Rat Skeletal Muscle

scholarly journals Hypertrophy of Rat Skeletal Muscle Is Associated with Increased SIRT1/Akt/mTOR/S6 and Suppressed Sestrin2/SIRT3/FOXO1 Levels

2021 ◽  
Vol 22 (14) ◽  
pp. 7588
Author(s):  
Zoltan Gombos ◽  
Erika Koltai ◽  
Ferenc Torma ◽  
Peter Bakonyi ◽  
Attila Kolonics ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Male Rats ◽  
Cellular Interactions ◽  
Molecular Signaling ◽  
Protein Breakdown ◽  
Rat Skeletal Muscle ◽  
Plantaris Muscle ◽  
Skeletal Muscle Hypertrophy ◽  
Intensive Investigation

Despite the intensive investigation of the molecular mechanism of skeletal muscle hypertrophy, the underlying signaling processes are not completely understood. Therefore, we used an overload model, in which the main synergist muscles (gastrocnemius, soleus) of the plantaris muscle were surgically removed, to cause a significant overload in the remaining plantaris muscle of 8-month-old Wistar male rats. SIRT1-associated pro-anabolic, pro-catabolic molecular signaling pathways, NAD and H2S levels of this overload-induced hypertrophy were studied. Fourteen days of overload resulted in a significant 43% (p < 0.01) increase in the mass of plantaris muscle compared to sham operated animals. Cystathionine-β-synthase (CBS) activities and bioavailable H2S levels were not modified by overload. On the other hand, overload-induced hypertrophy of skeletal muscle was associated with increased SIRT1 (p < 0.01), Akt (p < 0.01), mTOR, S6 (p < 0.01) and suppressed sestrin 2 levels (p < 0.01), which are mostly responsible for anabolic signaling. Decreased FOXO1 and SIRT3 signaling (p < 0.01) suggest downregulation of protein breakdown and mitophagy. Decreased levels of NAD+, sestrin2, OGG1 (p < 0.01) indicate that the redox milieu of skeletal muscle after 14 days of overloading is reduced. The present investigation revealed novel cellular interactions that regulate anabolic and catabolic processes in the hypertrophy of skeletal muscle.

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