Abstract:Sarcopenia, also known as skeletal muscle atrophy, is characterized by significant loss of muscle mass and strength. Oyster (Crassostrea gigas) hydrolysates have anti-cancer, antioxidant, and anti-inflammation properties. However, the anti-sarcopenic effect of oyster hydrolysates remains uninvestigated. Therefore, we prepared two different oyster hydrolysates, namely TGPN and PNY. This study aimed to determine the anti-muscle atrophy efficacy and molecular mechanisms of TGPN and PNY on both C2C12 cell lines an… Show more
“…Specifically, the phosphorylation of mTORC1, S6K1, and 4E-BP1 was promoted to increase MPS, while MPD was inhibited by decreasing the experssion of MuRF1 and Atrogin-1 via the PI3K/Akt/FoxO3a pathway. Furthermore, TGPN and PNY activated mitochondrial biogenesis through the SIRT1/PGC-1α pathway in immobilization-induced muscle atrophy mice …”
Section: Mechanism Of Antisarcopenic
Peptides In Alleviating
Sarcopeniamentioning
confidence: 94%
“…80 Furthermore, the antisarcopenic effect of marine peptides was explored. Jeon and Choung 82 prepared two oyster (Crassostrea gigas) peptides, one of which hydrolyzed with transglutaminase, protamex, and Neutrase was called TGPN, while the other hydrolyzed with protamex, Neutrase and fermented by yeast was called PNY. They explored the antisarcopenic effect and molecular mechanism of TGPN and PNY using C57BL/6J mice.…”
Section: Antisarcopenic Peptides Derived From Somementioning
Sarcopenia is an age-related progressive
muscle disorder characterized
by accelerated loss of muscle mass, strength, and function, which
are important causes of physiological dysfunctions in the elderly.
At present, the main alleviating method includes protein supplements
to stimulate synthesis of muscle proteins. Food protein-derived peptides
containing abundant branched-chain amino acids have a remarkable effect
on the improvement of sarcopenia. Understanding the underlying molecular
mechanism and clarifying the structure–activity relationship
is essential for the mitigation of sarcopenia. This present review
recaps the epidemiology, pathogenesis, diagnosis, and treatment of
sarcopenia, which facilitates a comprehensive understanding of sarcopenia.
Moreover, the latest research progress on food-derived antisarcopenic
peptides is reviewed, including their antisarcopenic activity, molecular
mechanism as well as structural characteristics. Food-derived bioactive
peptides can indeed alleviate/mitigate sarcopenia. These antisarcopenic
peptides play a pivotal role mainly by activating the PI3K/Akt/mTOR
and MAPK pathways and inhibiting the ubiquitin-proteasome system and
AMPK pathway, thus promoting the synthesis of muscle proteins and
inhibiting their degradation. Antisarcopenic peptides alleviate sarcopenia via specific peptides, which may be absorbed into the circulation
and exhibit their bioactivity in intact forms. The present review
provides a theoretical reference for mitigation and prevention of
sarcopenia by food protein-derived bioactive peptides.
“…Specifically, the phosphorylation of mTORC1, S6K1, and 4E-BP1 was promoted to increase MPS, while MPD was inhibited by decreasing the experssion of MuRF1 and Atrogin-1 via the PI3K/Akt/FoxO3a pathway. Furthermore, TGPN and PNY activated mitochondrial biogenesis through the SIRT1/PGC-1α pathway in immobilization-induced muscle atrophy mice …”
Section: Mechanism Of Antisarcopenic
Peptides In Alleviating
Sarcopeniamentioning
confidence: 94%
“…80 Furthermore, the antisarcopenic effect of marine peptides was explored. Jeon and Choung 82 prepared two oyster (Crassostrea gigas) peptides, one of which hydrolyzed with transglutaminase, protamex, and Neutrase was called TGPN, while the other hydrolyzed with protamex, Neutrase and fermented by yeast was called PNY. They explored the antisarcopenic effect and molecular mechanism of TGPN and PNY using C57BL/6J mice.…”
Section: Antisarcopenic Peptides Derived From Somementioning
Sarcopenia is an age-related progressive
muscle disorder characterized
by accelerated loss of muscle mass, strength, and function, which
are important causes of physiological dysfunctions in the elderly.
At present, the main alleviating method includes protein supplements
to stimulate synthesis of muscle proteins. Food protein-derived peptides
containing abundant branched-chain amino acids have a remarkable effect
on the improvement of sarcopenia. Understanding the underlying molecular
mechanism and clarifying the structure–activity relationship
is essential for the mitigation of sarcopenia. This present review
recaps the epidemiology, pathogenesis, diagnosis, and treatment of
sarcopenia, which facilitates a comprehensive understanding of sarcopenia.
Moreover, the latest research progress on food-derived antisarcopenic
peptides is reviewed, including their antisarcopenic activity, molecular
mechanism as well as structural characteristics. Food-derived bioactive
peptides can indeed alleviate/mitigate sarcopenia. These antisarcopenic
peptides play a pivotal role mainly by activating the PI3K/Akt/mTOR
and MAPK pathways and inhibiting the ubiquitin-proteasome system and
AMPK pathway, thus promoting the synthesis of muscle proteins and
inhibiting their degradation. Antisarcopenic peptides alleviate sarcopenia via specific peptides, which may be absorbed into the circulation
and exhibit their bioactivity in intact forms. The present review
provides a theoretical reference for mitigation and prevention of
sarcopenia by food protein-derived bioactive peptides.
“…Skeletal muscle atrophy involves several signal pathways such as ubiquitin proteasome system and autophagy lysosome system (Shen et al, 2019;Wu et al, 2019;Ma et al, 2021;Wang et al, 2022b). Skeletal muscle atrophy is also related to mitochondrial function, and regulating mitochondrial biogenesis can improve resistance to muscle atrophy (Shen et al, 2020;Jeon and Choung, 2021). When mitochondria are dysfunctional, increased intracellular ROS level activates apoptosis-related signaling pathways and the degradation of many proteins (Theilen et al, 2017).…”
Section: The Role Of Mitochondria In Muscle Atrophymentioning
confidence: 99%
“…Skeletal muscle atrophy is also related to mitochondrial function, and regulating mitochondrial biogenesis can improve resistance to muscle atrophy ( Shen et al, 2020 ; Jeon and Choung, 2021 ). When mitochondria are dysfunctional, increased intracellular ROS level activates apoptosis-related signaling pathways and the degradation of many proteins ( Theilen et al, 2017 ).…”
Section: The Role Of Mitochondria In Myogenesis Regeneration and Musc...mentioning
Skeletal muscle is one of the largest organs in the body and the largest protein repository. Mitochondria are the main energy-producing organelles in cells and play an important role in skeletal muscle health and function. They participate in several biological processes related to skeletal muscle metabolism, growth, and regeneration. Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor and regulator of systemic energy balance. AMPK is involved in the control of energy metabolism by regulating many downstream targets. In this review, we propose that AMPK directly controls several facets of mitochondrial function, which in turn controls skeletal muscle metabolism and health. This review is divided into four parts. First, we summarize the properties of AMPK signal transduction and its upstream activators. Second, we discuss the role of mitochondria in myogenesis, muscle atrophy, regeneration post-injury of skeletal muscle cells. Third, we elaborate the effects of AMPK on mitochondrial biogenesis, fusion, fission and mitochondrial autophagy, and discuss how AMPK regulates the metabolism of skeletal muscle by regulating mitochondrial function. Finally, we discuss the effects of AMPK activators on muscle disease status. This review thus represents a foundation for understanding this biological process of mitochondrial dynamics regulated by AMPK in the metabolism of skeletal muscle. A better understanding of the role of AMPK on mitochondrial dynamic is essential to improve mitochondrial function, and hence promote skeletal muscle health and function.
“…Substances with this potential activity include proteins and peptides present in protein hydrolysates [10]. Moreover, oyster hydrolysate [11], potato protein hydrolysate [12], and collagen hydrolysate [13] exhibit muscle atrophy-inhibitory effects. In particular, proteins and peptides of marine origin possess this potential biological activity.…”
Loss of muscle mass is the primary symptom of sarcopenia. Protein intake is recommended to prevent muscle mass loss, and Spirulina platensis, a microalga with high protein content, is a potential protein supplement. Here, we evaluated the differentiation ability of C2C12 cells and the inhibitory effect of Spirulina hydrolysates (SPH) prepared by Collupulin on dexamethasone (DEX)-treated C2C12 cells. SPH contained 578.27 mg/g protein and 92.30 mg/g branched-chain amino acids. SPH increased C2C12 myotube length and diameter, likely owing to increased MyoD1 and Myf5 expression. Inhibition of increased Atrogin-1, MuRF-1, and FoxO3 expression by SPH in DEX-treated C2C12 cells suppressed DEX-induced muscle atrophy. Moreover, SPH inhibited the DEX-induced increase in cytosolic p-Akt protein expression and suppressed the increase in nuclear FoxO3a protein expression, thereby suppressing the increase in the protein expression of the ubiquitin-proteasome-related factors Atrogin-1 and MuRF-1, which are involved in muscle atrophy. SPH suppressed DEX-induced muscle atrophy by activating the Akt/FoxO3a pathway. SPH promoted C2C12 myoblast differentiation into myotubes and inhibited DEX-induced myotube atrophy by suppressing Atrogin-1 and MuRF-1 expression and regulating the FoxO3a transcription factor. Collectively, SPH can be used as a functional food to inhibit muscle atrophy and promote muscle regeneration.
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