Insulin/IGF1 signalling mediates the effects of β
Adrenergic beta-2 Receptor Agonists
/ pharmacology
Animals
Autophagy
/ drug effects
Insulin
/ metabolism
Insulin-Like Growth Factor I
/ metabolism
Lysosomes
/ metabolism
Male
Mice
Mice, Knockout
Muscle Proteins
/ metabolism
Muscle Strength
Muscle, Skeletal
/ drug effects
Phosphatidylinositol 3-Kinases
Proteolysis
Proteostasis
/ drug effects
Proto-Oncogene Proteins c-akt
/ metabolism
Signal Transduction
/ drug effects
Autophagy-lysosomal system
Insulin/IGF1 signalling
Protein metabolism
Skeletal muscle function
Skeletal muscle plasticity
β2-adrenoceptor
Journal
Journal of cachexia, sarcopenia and muscle
ISSN: 2190-6009
Titre abrégé: J Cachexia Sarcopenia Muscle
Pays: Germany
ID NLM: 101552883
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
15
05
2018
accepted:
18
12
2018
pubmed:
2
4
2019
medline:
4
6
2020
entrez:
2
4
2019
Statut:
ppublish
Résumé
Stimulation of β Fed wild type (WT), 2-day fasted WT, muscle-specific insulin (INS) receptor (IR) knockout (M-IR In fed and fasted mice, one injection of FOR inhibited autophagosome formation (LC3-II content, 65%, P ≤ 0.05) that was paralleled by an increase in serum INS levels (4-fold to 25-fold, P ≤ 0.05) and the phosphorylation of Akt (4.4-fold to 6.5-fold, P ≤ 0.05) and ERK1/2 (50% to two-fold, P ≤ 0.05). This led to the suppression (40-70%, P ≤ 0.05) of the master regulators of atrophy, FoxOs, and the mRNA levels of their target genes. FOR enhanced (41%, P ≤ 0.05) protein synthesis only in fed condition and stimulated (4.4-fold to 35-fold, P ≤ 0.05) the prosynthetic Akt/mTOR/p70S6K pathway in both fed and fasted states. FOR effects on Akt signalling during fasting were blunted in both M-IR NS/IGF1 signalling is necessary for the anti-proteolytic and hypertrophic effects of in vivo β
Sections du résumé
BACKGROUND
Stimulation of β
METHODS
Fed wild type (WT), 2-day fasted WT, muscle-specific insulin (INS) receptor (IR) knockout (M-IR
RESULTS
In fed and fasted mice, one injection of FOR inhibited autophagosome formation (LC3-II content, 65%, P ≤ 0.05) that was paralleled by an increase in serum INS levels (4-fold to 25-fold, P ≤ 0.05) and the phosphorylation of Akt (4.4-fold to 6.5-fold, P ≤ 0.05) and ERK1/2 (50% to two-fold, P ≤ 0.05). This led to the suppression (40-70%, P ≤ 0.05) of the master regulators of atrophy, FoxOs, and the mRNA levels of their target genes. FOR enhanced (41%, P ≤ 0.05) protein synthesis only in fed condition and stimulated (4.4-fold to 35-fold, P ≤ 0.05) the prosynthetic Akt/mTOR/p70S6K pathway in both fed and fasted states. FOR effects on Akt signalling during fasting were blunted in both M-IR
CONCLUSIONS
NS/IGF1 signalling is necessary for the anti-proteolytic and hypertrophic effects of in vivo β
Identifiants
pubmed: 30932373
doi: 10.1002/jcsm.12395
pmc: PMC6463755
doi:
Substances chimiques
Adrenergic beta-2 Receptor Agonists
0
Insulin
0
Muscle Proteins
0
Insulin-Like Growth Factor I
67763-96-6
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
455-475Subventions
Organisme : NIDDK NIH HHS
ID : K08 DK100543
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK036836
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK055545
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK033201
Pays : United States
Informations de copyright
© 2019 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders.
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