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Nutrition and Regulation of Muscle Protein Synthesis

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Sports Nutrition".

Deadline for manuscript submissions: closed (20 May 2023) | Viewed by 34384

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Dr. Sara Salucci

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Cellular Signalling Laboratory, Department of Biomedical and NeuroMotor Sciences (DIBINEM), University of Bologna, 40126 Bologna, Italy
Interests: skeletal muscle disorders; apoptosis; autophagy; mitochondria behavior; antioxidants
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Dear Colleagues,

Skeletal muscle is a crucial tissue for human health since it controls several metabolic activities, including thermal regulation, nutritional balance, glucose uptake, and the endocrine system. Alterations in body glucose homeostasis, falls, fractures, disability, and chronic diseases are associated with loss of skeletal muscle mass. Protein synthesis and degradation are two important regulated processes that act in concert to maintain muscle mass. In atrophic conditions, protein synthesis impairment is associated with several conditions, including physical inactivity, sarcopenia, aging- and muscle-wasting-related diseases, as well as malnutrition, corticosteroid therapies, or inflammation. The availability of nutrients is one of the factors which can influence protein turnover. In fact, when muscle protein breakdown exceeds the rate of muscle protein synthesis, loss of protein occurs involving the ubiquitin-proteasomal system, autophagy, and the calpain signaling. The knowledge of these pathways helps to understand their role in muscle remodeling and in response to diet, knowing that a balanced nutrition intake represents a potential clinical intervention to reactivate protein synthesis during atrophy. The aim of this Special Issue is to collect original articles or reviews which discuss the therapeutic strategies, based on current nutrition interventions, able to modulate muscle protein turnover in muscle wasting conditions.

Dr. Sara Salucci
Guest Editor

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Keywords

skeletal muscle disorders
protein synthesis
protein degradation
nutrition
micronutrients and macronutrients

Published Papers (10 papers)

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Editorial

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3 pages, 200 KiB

Open AccessEditorial

Nutrition and Regulation of Muscle Protein Synthesis

by Sara Salucci

Nutrients 2023, 15(18), 4017; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15184017 - 16 Sep 2023

Viewed by 1227

Abstract

Skeletal muscles are an indispensable actor for daily activities, playing an essential role in locomotion through both the control of posture and position and by joint stabilization [...] Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

Research

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18 pages, 3590 KiB

Open AccessArticle

The Cytotoxic Effect of Curcumin in Rhabdomyosarcoma Is Associated with the Modulation of AMPK, AKT/mTOR, STAT, and p53 Signaling

by Sara Salucci, Alberto Bavelloni, Anna Bartoletti Stella, Francesco Fabbri, Ivan Vannini, Manuela Piazzi, Karyna Volkava, Katia Scotlandi, Giovanni Martinelli, Irene Faenza and William Blalock

Nutrients 2023, 15(3), 740; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15030740 - 01 Feb 2023

Cited by 5 | Viewed by 2208

Abstract

Approximately 7% of cancers arising in children and 1% of those arising in adults are soft tissue sarcomas (STS). Of these malignancies, rhabdomyosarcoma (RMS) is the most common. RMS survival rates using current therapeutic protocols have remained largely unchanged in the past decade. Thus, it is imperative that the main molecular drivers in RMS tumorigenesis are defined so that more precise, effective, and less toxic therapies can be designed. Curcumin, a common herbal supplement derived from plants of the Curcuma longa species, has an exceptionally low dietary biotoxicity profile and has demonstrated anti-tumorigenic benefits in vitro. In this study, the anti-tumorigenic activity of curcumin was assessed in rhabdomyosarcoma cell lines and used to identify the major pathways responsible for curcumin’s anti-tumorigenic effects. Curcumin treatment resulted in cell cycle arrest, inhibited cell migration and colony forming potential, and induced apoptotic cell death. Proteome profiler array analysis demonstrated that curcumin treatment primarily influenced flux through the AKT-mammalian target of rapamycin (mTOR), signal transducer and activator of transcription (STAT), AMP-dependent kinase (AMPK), and p53 associated pathways in a rhabdomyosarcoma subtype-specific manner. Thus, the strategic, combinational therapeutic targeting of these pathways may present the best option to treat this group of tumors. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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11 pages, 32158 KiB

Open AccessArticle

The Administration of Panax Ginseng Berry Extract Attenuates High-Fat-Diet-Induced Sarcopenic Obesity in C57BL/6 Mice

by Ji-Eun Shin, So-Hyun Jeon, Sang-Jun Lee and Se-Young Choung

Nutrients 2022, 14(9), 1747; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14091747 - 22 Apr 2022

Cited by 8 | Viewed by 2407

Abstract

Sarcopenia and obesity are serious health problems that are highly related to several metabolic diseases. Sarcopenic obesity, a combined state of sarcopenia and obesity, results in higher risks of metabolic diseases and even mortality than sarcopenia or obesity alone. Therefore, the development of therapeutic agents for sarcopenic obesity is crucial. C57BL/6 mice were fed with a high-fat diet (HFD) for 9 weeks. Then, mice were administered with Panax ginseng berry extract (GBE) for an additional 4 weeks, with continuous HFD intake. GBE significantly decreased the food efficiency ratio, serum lipid and insulin levels, adipose tissue weights, and adipocyte size. It significantly increased the grip strength, muscle masses, and myofiber cross-sectional area. It deactivated the protein kinase C (PKC) theta and zeta, resulting in activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway, which is known to regulate muscle synthesis and degradation. Furthermore, it inhibited the production of inflammatory cytokines in the muscle tissue. GBE attenuated both obesity and sarcopenia. Thus, GBE is a potential agent to prevent or treat sarcopenic obesity. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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19 pages, 3262 KiB

Open AccessArticle

Satellite Cells Exhibit Decreased Numbers and Impaired Functions on Single Myofibers Isolated from Vitamin B6-Deficient Mice

by Takumi Komaru, Noriyuki Yanaka and Thanutchaporn Kumrungsee

Nutrients 2021, 13(12), 4531; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124531 - 17 Dec 2021

Cited by 4 | Viewed by 3233

Abstract

Emerging research in human studies suggests an association among vitamin B6, sarcopenia, and muscle strength. However, very little is known regarding its potential role at the cellular level, especially in muscle satellite cells. Therefore, to determine whether vitamin B6 affects the satellite cells, we isolated single myofibers from muscles of vitamin B6-deficient and vitamin B6-supplemented mice. Subsequently, we subjected them to single myofiber culture and observed the number and function of the satellite cells, which remained in their niche on the myofibers. Prior to culture, the vitamin B6-deficient myofibers exhibited a significantly lower number of quiescent satellite cells, as compared to that in the vitamin B6-supplemented myofibers, thereby suggesting that vitamin B6 deficiency induces a decline in the quiescent satellite cell pool in mouse muscles. After 48 and 72 h of culture, the number of proliferating satellite cells per cluster was similar between the vitamin B6-deficient and -supplemented myofibers, but their numbers decreased significantly after culturing the myofibers in vitamin B6-free medium. After 72 h of culture, the number of self-renewing satellite cells per cluster was significantly lower in the vitamin B6-deficient myofibers, and the vitamin B6-free medium further decreased this number. In conclusion, vitamin B6 deficiency appears to reduce the number of quiescent satellite cells and suppress the proliferation and self-renewal of satellite cells during myogenesis. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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16 pages, 3416 KiB

Open AccessArticle

Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice

by So-Hyun Jeon and Se-Young Choung

Nutrients 2021, 13(12), 4385; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124385 - 08 Dec 2021

Cited by 17 | Viewed by 4841

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 and mice. In vitro, the TGPN and PNY recovered the dexamethasone-induced reduction in the myotube diameters. In vivo, TGPN and PNY administration not only improved grip strength and exercise endurance, but also attenuated the loss of muscle mass and muscle fiber cross-sectional area. Mechanistically, TGPN and PNY increased the expression of protein synthesis-related protein levels via phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of the rapamycin pathway, and reduced the expression of protein degradation-related protein levels via the PI3K/Akt/forkhead box O pathway. Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1α signaling. These findings suggest oyster hydrolysates could be used as a valuable natural material that inhibits skeletal muscle atrophy via regulating protein turnover and mitochondrial biogenesis. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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17 pages, 2069 KiB

Open AccessArticle

A Bioassay-Guided Fractionation of Rosemary Leaf Extract Identifies Carnosol as a Major Hypertrophy Inducer in Human Skeletal Muscle Cells

by Sylvie Morel, Gérald Hugon, Manon Vitou, Marie Védère, Françoise Fons, Sylvie Rapior, Nathalie Saint and Gilles Carnac

Nutrients 2021, 13(12), 4190; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124190 - 23 Nov 2021

Cited by 5 | Viewed by 2932

Abstract

A good quality of life requires maintaining adequate skeletal muscle mass and strength, but therapeutic agents are lacking for this. We developed a bioassay-guided fractionation approach to identify molecules with hypertrophy-promoting effect in human skeletal muscle cells. We found that extracts from rosemary leaves induce muscle cell hypertrophy. By bioassay-guided purification we identified the phenolic diterpene carnosol as the compound responsible for the hypertrophy-promoting activity of rosemary leaf extracts. We then evaluated the impact of carnosol on the different signaling pathways involved in the control of muscle cell size. We found that activation of the NRF2 signaling pathway by carnosol is not sufficient to mediate its hypertrophy-promoting effect. Moreover, carnosol inhibits the expression of the ubiquitin ligase E3 Muscle RING Finger protein-1 that plays an important role in muscle remodeling, but has no effect on the protein synthesis pathway controlled by the protein kinase B/mechanistic target of rapamycin pathway. By measuring the chymotrypsin-like activity of the proteasome, we found that proteasome activity was significantly decreased by carnosol and Muscle RING Finger 1 inactivation. These results strongly suggest that carnosol can induce skeletal muscle hypertrophy by repressing the ubiquitin-proteasome system-dependent protein degradation pathway through inhibition of the E3 ubiquitin ligase Muscle RING Finger protein-1. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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20 pages, 3940 KiB

Open AccessArticle

Egg White Protein Feeding Facilitates Skeletal Muscle Gain in Young Rats with/without Clenbuterol Treatment

by Keiichi Koshinaka, Asuka Honda, Rihei Iizumi, Yuto Miyazawa, Kentaro Kawanaka and Akiko Sato

Nutrients 2021, 13(6), 2042; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13062042 - 15 Jun 2021

Cited by 4 | Viewed by 3724

Abstract

Based on the Digestible Indispensable Amino Acid Score (DIAAS), egg white protein (EGG) has an excellent score, comparable to that of whey protein but with a lower amount of leucine. We examined the effect of EGG feeding on rat skeletal muscle gain in comparison to that of two common animal-derived protein sources: casein (CAS) and whey (WHE). To explore the full potential of EGG, this was examined in clenbuterol-treated young rats. Furthermore, we focused on leucine-associated anabolic signaling in response to EGG after single-dose ingestion and chronic ingestion, as well as clenbuterol treatment. Because EGG is an arginine-rich protein source, a portion of the experiment was repeated with diets containing equal amounts of arginine. We demonstrated that EGG feeding accelerates skeletal muscle gain under anabolism-dominant conditions more efficiently than CAS and WHE and this stronger effect with EGG is not dependent on the arginine-rich composition of the protein source. We also demonstrated that the plausible mechanism of the stronger muscle-gain effect with EGG is not detectable in the mechanistic target of rapamycin (mTOR) or insulin signaling under our experimental conditions. We conclude that EGG may have a superior efficiency in muscle gain compared to other common animal-based proteins. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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16 pages, 2030 KiB

Open AccessArticle

A Fish-Derived Protein Hydrolysate Induces Postprandial Aminoacidaemia and Skeletal Muscle Anabolism in an In Vitro Cell Model Using Ex Vivo Human Serum

by Matthew J. Lees, David Nolan, Miryam Amigo-Benavent, Conor J. Raleigh, Neda Khatib, Pádraigín Harnedy-Rothwell, Richard J. FitzGerald, Brendan Egan and Brian P. Carson

Nutrients 2021, 13(2), 647; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020647 - 17 Feb 2021

Cited by 7 | Viewed by 3814

Abstract

Fish-derived proteins, particularly fish protein hydrolysates (FPH), offer potential as high-quality sources of dietary protein, whilst enhancing economic and environmental sustainability. This study investigated the impact of a blue whiting-derived protein hydrolysate (BWPH) on aminoacidaemia in vivo and skeletal muscle anabolism in vitro compared with whey protein isolate (WPI) and an isonitrogenous, non-essential amino acid (NEAA) control (0.33 g·kg⁻¹·body mass⁻¹) in an ex vivo, in vitro experimental design. Blood was obtained from seven healthy older adults (two males, five females; age: 72 ± 5 years, body mass index: 24.9 ± 1.6 kg·m²) in three separate trials in a randomised, counterbalanced, double-blind design. C2C12 myotubes were treated with ex vivo human serum-conditioned media (20%) for 4 h. Anabolic signalling (phosphorylation of mTOR, p70S6K, and 4E-BP1) and puromycin incorporation were determined by immunoblotting. Although BWPH and WPI both induced postprandial essential aminoacidaemia in older adults above the NEAA control, peak and area under the curve (AUC) leucine and essential amino acids were more pronounced following WPI ingestion. Insulin was elevated above baseline in WPI and BWPH only, a finding reinforced by higher peak and AUC values compared with NEAA. Muscle protein synthesis, as measured by puromycin incorporation, was greater after incubation with WPI-fed serum compared with fasted serum (P = 0.042), and delta change was greater in WPI (P = 0.028) and BWPH (P = 0.030) compared with NEAA. Myotube hypertrophy was greater in WPI and BWPH compared with NEAA (both P = 0.045), but was similar between bioactive conditions (P = 0.853). Taken together, these preliminary findings demonstrate the anabolic potential of BWPH in vivo and ex vivo, thus providing justification for larger studies in older adults using gold-standard measures of acute and chronic MPS in vivo. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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Review

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14 pages, 570 KiB

Open AccessReview

Nutritional Strategies to Prevent Muscle Loss and Sarcopenia in Chronic Kidney Disease: What Do We Currently Know?

by Giulia Massini, Lara Caldiroli, Paolo Molinari, Francesca Maria Ida Carminati, Giuseppe Castellano and Simone Vettoretti

Nutrients 2023, 15(14), 3107; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15143107 - 11 Jul 2023

Cited by 7 | Viewed by 3826

Abstract

Loss of muscle mass is an extremely frequent complication in patients with chronic kidney disease (CKD). The etiology of muscle loss in CKD is multifactorial and may depend on kidney disease itself, dialysis, the typical chronic low-grade inflammation present in patients with chronic kidney disease, but also metabolic acidosis, insulin resistance, vitamin D deficiency, hormonal imbalances, amino acid loss during dialysis, and reduced dietary intake. All these conditions together increase protein degradation, decrease protein synthesis, and lead to negative protein balance. Aging further exacerbates sarcopenia in CKD patients. Nutritional therapy, such as protein restriction, aims to manage uremic toxins and slow down the progression of CKD. Low-protein diets (LPDs) and very low-protein diets (VLPDs) supplemented with amino acids or ketoacids are commonly prescribed. Energy intake is crucial, with a higher intake associated with maintaining a neutral or positive nitrogen balance. Adequate nutritional and dietary support are fundamental in preventing nutritional inadequacies and, consequently, muscle wasting, which can occur in CKD patients. This review explores the causes of muscle loss in CKD and how it can be influenced by nutritional strategies aimed at improving muscle mass and muscle strength. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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16 pages, 2444 KiB

Open AccessReview

Extra Virgin Olive Oil (EVOO), a Mediterranean Diet Component, in the Management of Muscle Mass and Function Preservation

by Sara Salucci, Anna Bartoletti-Stella, Alberto Bavelloni, Beatrice Aramini, William L. Blalock, Francesco Fabbri, Ivan Vannini, Vittorio Sambri, Franco Stella and Irene Faenza

Nutrients 2022, 14(17), 3567; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14173567 - 30 Aug 2022

Cited by 14 | Viewed by 3994

Abstract

Aging results in a progressive decline in skeletal muscle mass, strength and function, a condition known as sarcopenia. This pathological condition is due to multifactorial processes including physical inactivity, inflammation, oxidative stress, hormonal changes, and nutritional intake. Physical therapy remains the standard approach to treat sarcopenia, although some interventions based on dietary supplementation are in clinical development. In this context, thanks to its known anti-inflammatory and antioxidative properties, there is great interest in using extra virgin olive oil (EVOO) supplementation to promote muscle mass and health in sarcopenic patients. To date, the molecular mechanisms responsible for the pathological changes associated with sarcopenia remain undefined; however, a complete understanding of the signaling pathways that regulate skeletal muscle protein synthesis and their behavior during sarcopenia appears vital for defining how EVOO might attenuate muscle wasting during aging. This review highlights the main molecular players that control skeletal muscle mass, with particular regard to sarcopenia, and discusses, based on the more recent findings, the potential of EVOO in delaying/preventing loss of muscle mass and function, with the aim of stimulating further research to assess dietary supplementation with EVOO as an approach to prevent or delay sarcopenia in aging individuals. Full article

(This article belongs to the Special Issue Nutrition and Regulation of Muscle Protein Synthesis)

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