| Summary: | Exercise mimetics are pharmacological compounds that trigger pathways similar to those activated as a consequence of exercise training. They are therefore useful in pathological conditions where physical activity is beneficial but unfeasible. Models of exercise mimetics can also be used to study the targets implicated in training or conversely, inactivity. In the study presented insulin-like growth factor-1 (IGF-1) is investigated as an in vitro model of exercise mimetics, plus or minus the addition of Exo1 drug, that should impair the crosstalk between endoplasmic reticulum and the Golgi apparatus to inquire in its role in exercise metabolism
In this study, cultures from the murine musculoskeletal cell line C2C12 are divided into three experimental groups for each exercise mimetics: a control group, a treated group and a treated group plus Exo1. Cells are treated for 24h and 48h.
IGF-1 increased myotube width at 24h by eliciting mTORC2, followed by mTORC1 at 48h. Hypertrophy was achieved independently of pMAPK.
IGF-1 overcompensated for Exo1-caused ER stress by inducing hypertrophy at 24h, but the effect was impaired after 48h. Hypertrophy at 24h was achieved through phosphorylation of ERK1/2 and pAkt.
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