Effects of short-term fasting on the Akt-mediated pathway involved in protein metabolism in chicken skeletal muscle

Saneyasu, Takaoki; Tsuchii, Nami; Nakano, Yuma; Kitashiro, Ayana; Tsuchihashi, Tatsuya; Shindo, Haruka; Honda, Kazuhisa; Kamisoyama, Hiroshi

doi:10.1016/j.domaniend.2017.06.002

Cited by 9 publications

(10 citation statements)

References 33 publications

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“…In addition, fasting inhibits mTOR activity (phosphorylation of S6K1and 4E-BP1) in mouse skeletal muscles (Mammucari et al, 2007). Fasting also decreases the phosphorylation of S6 ribosomal protein downstream of S6K1, a maker of mTOR activity, in skeletal muscles (Shavlakadze et al, 2013;Saneyasu et al, 2017). In this study, fasting also inhibited AKT and mTOR signaling in chick skeletal muscle.…”

Section: Resultssupporting

confidence: 57%

“…3A. We used fasting as an approached for mTOR inhibition in skeletal muscle since it is an established condition that inhibits phosphorylation of mTOR target proteins (Mammucari et al, 2007;Naito et al, 2013;Shavlakadze et al, 2013;Saneyasu et al, 2017). The phosphorylation of AKT (Ser473), p70 ribosomal S6 kinase 1 (S6K1, Thr389), S6 ribosomal protein (Ser235/236), and 4E-BP1(Thr37/46) was inhibited by fasting, thereby that fasting inhibited AKT and mTOR signaling (phosphorylation of S6K1, S6 ribosomal protein, and 4E-BP1).…”

Section: Resultsmentioning

confidence: 99%

“…Activation of mTOR signaling downstream of AKT stimulates protein synthesis and inhibits protein degradation by phosphorylating two major targets, S6K1 and 4E-BP1. Fasting inhibits the phosphorylation of AKT in mouse and chicken skeletal muscles (Mammucari et al, 2007;Shavlakadze et al, 2013;Saneyasu et al, 2017). In addition, fasting inhibits mTOR activity (phosphorylation of S6K1and 4E-BP1) in mouse skeletal muscles (Mammucari et al, 2007).…”

Section: Resultsmentioning

confidence: 99%

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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: Resultssupporting

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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

Nakashima

Ishida

2020

J. Poult. Sci.

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“…The hypothalamus was dissected, immediately frozen in liquid nitrogen, and stored at −80℃. Western blot analysis was performed as previously reported (Saneyasu et al, 2017). The frozen hypothalamus was ultrasonicated in a lysis buffer.…”

Section: Experiments 2 Effect Of Central Administration Of Igf-1 On Tmentioning

confidence: 99%

Role of Insulin-like Growth Factor-1 in the Central Regulation of Feeding Behavior in Chicks

et al. 2019

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Insulin-like growth factor-1 (IGF-1) is a key regulator of muscle development and metabolism in chickens. Recently, we have demonstrated that intracerebroventricular administration of IGF-1 significantly decreased food intake in broiler chicks. However, the molecular mechanisms underlying the IGF-1-induced anorexia and the anorexigenic effect of IGF-1 in different strains of commercial chicks have not been investigated. Neuropeptide Y (NPY, a hypothalamic orexigenic neuropeptide), agouti-related protein (AgRP, a hypothalamic orexigenic neuropeptide), and proopiomelanocortin (POMC, the precursor of hypothalamic anorexigenic neuropeptides) play important roles in the regulation of food intake in both mammals and chickens. Evidence shows that several cell signaling pathways in the hypothalamus are involved in regulating the feeding behavior of mammals. In the present study, we first investigated the effects of IGF-1 on the expression of appetite-regulating neuropeptides and phosphorylation of signaling molecules in the hypothalamus of broiler chicks. Intracerebroventricular administration of IGF-1 significantly increased the mRNA levels of POMC, whereas the mRNA levels of NPY and AgRP were not significantly altered. IGF-1 also significantly induced the phosphorylation of v-Akt murine thymoma viral oncogene homolog 1 (AKT) in the hypothalamus of chicks, but did not influence the phosphorylation of forkhead box O1, S6 protein, AMP-activated protein kinase, and extracellular signal-regulated kinase 1/2. We also compared the effect of IGF-1 on food intake in broiler chicks (a hyperphagic strain of chickens) and layer chicks. Results demonstrated that the threshold of IGF-1-induced anorexia in broiler chicks was higher than that in layer chicks. Our observations suggest that hypothalamic POMC and AKT may be involved in the IGF-1-induced anorexigenic pathway and that high threshold of IGF-1-induced anorexia in broiler chicks might be one of the causes of hyperphagia in broiler chicks. Overall, it appears that IGF-1 plays important roles in the central regulation of feeding behavior in chicks.

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“…Western blot analysis was performed as previously described by Saneyasu et al (2017). Briefly, cells were rinsed with ice-cold PBS.…”

Section: Western Blot Analysismentioning

confidence: 99%

Myostatin Increases Smad2 Phosphorylation and Atrogin-1 Expression in Chick Embryonic Myotubes

2019

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Skeletal muscle mass is an important trait in poultry meat production. In mammals, myostatin, a negative regulator of skeletal muscle growth, activates Smad transcription factors and induces the expression of atrogin-1 by regulating the Akt/FOXO pathway. Although the amino acid sequence of chicken myostatin is known to be completely identical to its mammalian counterpart, previous studies in chicken skeletal muscles have implied that the physiological roles of chicken myostatin are different from those of mammals. Furthermore, it remains to be elucidated whether myostatin affects cellular signaling factors and atrogin-1 expression. In this study, using chick embryonic myotubes, we found that myostatin significantly increased the phosphorylation rate of Smad2 and mRNA levels of atrogin-1. No significant change was observed in the phosphorylation of Akt and FOXO1. These in vitro results suggest that the molecular mechanisms underlying myostatin-induced expression of atrogin-1 might be different between chickens and mammals.

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Effects of short-term fasting on the Akt-mediated pathway involved in protein metabolism in chicken skeletal muscle

Cited by 9 publications

References 33 publications

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

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

Role of Insulin-like Growth Factor-1 in the Central Regulation of Feeding Behavior in Chicks

Myostatin Increases Smad2 Phosphorylation and Atrogin-1 Expression in Chick Embryonic Myotubes

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