Regulation of Autophagy in Chick Myotubes: Effects of Insulin, Insulin-Like Growth Factor-I, and Amino Acids

Nakashima, Kazuki; Ishida, Aiko

doi:10.2141/jpsa.0170196

Cited by 6 publications

(6 citation statements)

References 29 publications

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“…Conversely, lack of nutrients or growth factors and low energy levels in the skeletal muscle induces autophagy (Sandri, 2008). We have previously reported that insulin, insulin-like growth factor-I, and amino acids suppress autophagy in chick myotubes (Nakashima and Ishida, 2018). This study showed that inhibition of mTOR induces autophagy in chick skeletal muscle.…”

Section: Resultsmentioning

confidence: 60%

Regulation of Autophagy in Chick Skeletal Muscle: Effect of mTOR Inhibition

Nakashima

Ishida

2020

J. Poult. Sci.

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Autophagy in the skeletal muscle increases under catabolic conditions resulting in muscle atrophy. This study investigated the effect of inhibition of mechanistic target of rapamycin (mTOR) on autophagy in chick skeletal muscle. We examined the effects of Torin1, an mTOR inhibitor, on autophagy. Chick myotubes were incubated with Torin1 (100 nM) for 3 h. It was observed that Torin1 inhibited the phosphorylation of AKT (Ser473), p70 ribosomal S6 kinase 1 (S6K1, Thr389), S6 ribosomal protein (Ser235/236), and eukaryotic translation initiation factor 4Ebinding protein 1 (4E-BP1, Thr37/46), which are used for measurement of mTOR activity. Torin1 significantly (P＜ 0.01) increased the LC3-II/LC3-I ratio, an index for autophagosome formation, while it did not influence the expression of autophagy-related genes (LC3B, GABARAPL1, and ATG12). In addition, Torin1 increased atrogin-1/ MAFbx (a muscle-specific ubiquitin ligase) mRNA expression. Fasting for 24 h inhibited the phosphorylation of AKT (Ser473), S6K1 (Ther389), S6 ribosomal protein (Ser235/236), and 4E-BP1 (Thr37/46) in chick skeletal muscle and significantly (P＜0.01) increased the LC3-II/LC3-I ratio. Fasting also increased GABARAPL1 and atrogin-1/MAFbx mRNA expression but not LC3B or ATG12 mRNA expression. These results indicate that mTOR signaling regulates autophagy and the ubiquitin-proteasome proteolytic pathway in chick skeletal muscle.

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Section: Resultsmentioning

confidence: 60%

Regulation of Autophagy in Chick Skeletal Muscle: Effect of mTOR Inhibition

Nakashima

Ishida

2020

J. Poult. Sci.

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“…However, few studies have extensively analyzed the effect of IGF-1 in skeletal muscle autophagy, and conflicting evidence has been presented. Nakashima et al treated chicken myotubes with IGF-1 and found that LC3-I to LC3-II conversion, a critical step for autophagosome formation, was decreased [ 64 ]. In contrast, Ascenzi et al showed that LC3-I to LC3-II conversion, which is normally decreased during aging, was increased in mice with skeletal muscle-specific overexpression of IGF-1 [ 65 ].…”

Section: Muscle Protein Degradation: Autophagymentioning

confidence: 99%

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Yoshida

Delafontaine

2020

Cells

356

209

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Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.

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“…However, the myostatin knockout mouse model also suggested that IGF-1 could stimulate muscle hypertrophy in the absence of myostatin, indicating distinct mechanisms for myostatin and IGF-1 regulation of skeletal muscle mass (Hennebry et al, 2017). IGF-1 also promotes skeletal muscle growth through the PI3K/ Akt pathway in chickens (Deng et al, 2014;Yu et al, 2015;Nakashima and Ishida, 2018;Nakashima and Ishida, 2019). Even though the IGF-1 axis is a prime target for muscle remodeling in poultry (e.g., Tomas et al, 1998;Saneyasu et al, 2016;Saneyasu et al, 2017;Chen et al, 2018), the IGF-1 axis has received much less research attention in wild birds, with reference to muscle remodeling for phenotypic flexibility, compared with the myostatin signaling pathway.…”

Section: Igf-1 Signaling Pathwaymentioning

confidence: 99%

Skeletal muscle and metabolic flexibility in response to changing energy demands in wild birds

2022

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Phenotypically plastic responses of animals to adjust to environmental variation are pervasive. Reversible plasticity (i.e., phenotypic flexibility), where adult phenotypes can be reversibly altered according to prevailing environmental conditions, allow for better matching of phenotypes to the environment and can generate fitness benefits but may also be associated with costs that trade-off with capacity for flexibility. Here, we review the literature on avian metabolic and muscle plasticity in response to season, temperature, migration and experimental manipulation of flight costs, and employ an integrative approach to explore the phenotypic flexibility of metabolic rates and skeletal muscle in wild birds. Basal (minimum maintenance metabolic rate) and summit (maximum cold-induced metabolic rate) metabolic rates are flexible traits in birds, typically increasing with increasing energy demands. Because skeletal muscles are important for energy use at the organismal level, especially to maximum rates of energy use during exercise or shivering thermogenesis, we consider flexibility of skeletal muscle at the tissue and ultrastructural levels in response to variations in the thermal environment and in workloads due to flight exercise. We also examine two major muscle remodeling regulatory pathways: myostatin and insulin-like growth factor -1 (IGF-1). Changes in myostatin and IGF-1 pathways are sometimes, but not always, regulated in a manner consistent with metabolic rate and muscle mass flexibility in response to changing energy demands in wild birds, but few studies have examined such variation so additional study is needed to fully understand roles for these pathways in regulating metabolic flexibility in birds. Muscle ultrastrutural variation in terms of muscle fiber diameter and associated myonuclear domain (MND) in birds is plastic and highly responsive to thermal variation and increases in workload, however, only a few studies have examined ultrastructural flexibility in avian muscle. Additionally, the relationship between myostatin, IGF-1, and satellite cell (SC) proliferation as it relates to avian muscle flexibility has not been addressed in birds and represents a promising avenue for future study.

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Regulation of Autophagy in Chick Myotubes: Effects of Insulin, Insulin-Like Growth Factor-I, and Amino Acids

Cited by 6 publications

References 29 publications

Regulation of Autophagy in Chick Skeletal Muscle: Effect of mTOR Inhibition

Regulation of Autophagy in Chick Skeletal Muscle: Effect of mTOR Inhibition

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Skeletal muscle and metabolic flexibility in response to changing energy demands in wild birds

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