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Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies
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Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 1823

Special Issue Editor

Dr. Rasmus Kjøbsted

E-Mail Website
Guest Editor
Department of Nutrition, Exercise and Sports, University of Copenhagen, DK-2200 Copenhagen, Denmark
Interests: exercise; physical activity; skeletal muscle; energy metabolism; cellular signaling; metabolic disorders; tissue-specific drug targeting; drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle is not only essential for movement and posture, but it also plays a vital role in regulating whole-body metabolism. Accounting for ~40% of body mass, skeletal muscle is the primary site of insulin-mediated glucose disposal and a major contributor to resting energy expenditure. As such, any alterations in skeletal muscle function or metabolism can have profound implications for the development and progression of metabolic disorders.

Skeletal muscle is also a highly dynamic organ, capable of increasing energy turnover by more than 100-fold during exercise. This remarkable metabolic plasticity is underpinned by a complex network of intracellular signaling pathways that are responsive to a wide range of factors, including diet and exercise.

In recent years, skeletal muscle has also emerged as a major endocrine organ, releasing myokines that act on distant tissues to regulate metabolism, inflammation, and immunity. This role of skeletal muscle as an endocrine organ further underscores its critical importance for overall health and well-being.

The current Special Issue of the International Journal of Molecular Sciences is dedicated to exploring the latest advances in our understanding of skeletal muscle metabolism and its regulation by diet, exercise, and pharmacotherapies. The Special Issue features a collection of original research articles and review papers that highlight the complex interplay between these factors in shaping skeletal muscle function and metabolism in health and disease.

Specifically, the Special Issue covers a broad range of topics, including:

  • The molecular mechanisms by which diet, exercise, and pharmacotherapies regulate skeletal muscle metabolism;
  • The role of skeletal muscle metabolism in metabolic disorders such as obesity, type 2 diabetes, and sarcopenia;
  • The emerging role of skeletal muscle as an endocrine organ and the implications of myokines for health and disease;
  • The development of novel therapeutic strategies targeting skeletal muscle metabolism for the treatment of metabolic disorders.

I hope that this Special Issue will provide a valuable resource for researchers and clinicians interested in the field of skeletal muscle metabolism.

Dr. Rasmus Kjøbsted
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • energy metabolism
  • metabolic signaling pathways
  • metabolic homeostasis
  • metabolic disorders
  • muscle mass
  • muscle metabolites
  • diet
  • exercise
  • pharmacotherapies

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Related Special Issue

Published Papers (4 papers)

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Research

19 pages, 3205 KiB  
Article
MSTN Regulates Bovine Skeletal Muscle Satellite Cell Differentiation via PSMA6-Mediated AKT Signaling Pathway
by Tengxia Ma, Meiling Miao, Xiangquan Liu, Linlin Zhang, Yiwen Guo, Xin Li, Xiangbin Ding, Hong Guo and Debao Hu
Int. J. Mol. Sci. 2025, 26(11), 4963; https://doi.org/10.3390/ijms26114963 - 22 May 2025
Viewed by 157
Abstract
MSTN has been used as a candidate gene in the genetics, breeding, and improvement of animal breeds. However, the possible mechanism by which the MSTN gene regulates muscle development through PSMA6 is not well understood. Previous methylome and transcriptome sequencing analyses of gluteal [...] Read more.
MSTN has been used as a candidate gene in the genetics, breeding, and improvement of animal breeds. However, the possible mechanism by which the MSTN gene regulates muscle development through PSMA6 is not well understood. Previous methylome and transcriptome sequencing analyses of gluteal muscle tissues from MSTN+/−Luxi cattle and wild-type Luxi cattle identified that the PSMA6 gene exhibited a negative correlation between methylation levels and transcriptional activity. To investigate whether MSTN expression regulates PSMA6 gene expression, we examined the effects of MSTN on DNA methyltransferases (DNMT1, DNMT2, DNMT3A, and DNMT3B) and DNA demethylases (TET1, TET2, and TET3). Additionally, chromatin immunoprecipitation (ChIP) assays were performed to detect the binding interaction between PSMA6 and TET2. In this paper, we first established an MSTN knockdown cellular model to preliminarily validate its regulatory effect on PSMA6 expression. Subsequently, the developmental impact of PSMA6 on bovine skeletal muscle satellite cells was further investigated through both knockdown and overexpression of the PSMA6 gene. Furthermore, we examined changes in the expression of key components of the AKT/mTOR signaling pathway to elucidate the mechanisms underlying the PSMA6-mediated regulation of satellite cell development. The results demonstrate that myostatin (MSTN) inhibition significantly decreased proteasome 20S subunit alpha-6 (PSMA6) gene expression, while increasing demethylase expression, particularly ten-eleven translocation-2 (TET2), which exhibited the most pronounced changes. During the cell proliferation stage, the markers Paired Box 7 (PAX7) and Ki-67 exhibited no significant changes, whereas the PSMA6 gene was either overexpressed or disrupted. Conversely, PSMA6 overexpression altered the myogenic differentiation markers, causing the differential regulation of myosin heavy chain (MyHC) and myogenin (MyoG) expression, with MyHC upregulation and concurrent MyoG downregulation. PSMA6 gene overexpression led to the downregulation of AKT1 and Rac1, as well as the activation of the AKT/mTOR pathway, including key factors such as mTOR, p-mTOR, RPS6, p-RPS6, and RhoA. PSMA6 interference resulted in the downregulation of p-mTOR and the upregulation of p-RPS6. Gene expression profiling in our study revealed that the myostatin (MSTN) knockout model significantly reduced the transcriptional levels of the proteasome α6 subunit (PSMA6) (p < 0.05), with the regulatory intensity showing a significant negative correlation with MSTN expression. This molecular evidence substantiates a negative regulatory axis between MSTN and PSMA6. Functional experiments demonstrated that PSMA6 overexpression specifically enhanced myotube formation rates in bovine skeletal muscle satellite cells, whereas siRNA-mediated PSMA6 knockdown exhibited no significant effects on cellular proliferation, indicating the functional specificity of this gene in myogenic differentiation. Mechanistic investigations further revealed that PSMA6 activates the canonical AKT/mTOR signaling transduction cascade through the phosphorylation of AKT and its downstream effector mTOR, thereby mediating the expression of myogenic regulatory factors MyoD and myogenin. Collectively, these findings demonstrate that MSTN deficiency alleviates the transcriptional repression of PSMA6, remodels skeletal muscle differentiation-associated signaling networks, and ultimately drives the directional differentiation of satellite cells toward myofiber specification. Full article
(This article belongs to the Special Issue Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies)
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20 pages, 5346 KiB  
Article
Long-Term Moderate Increase in Medium-Chain Fatty Acids Intake Enhances Muscle Metabolism and Function in Mice
by Ziwei Zhang, Cong Wu, Shuo Wang, Yishan Tong, Jiapeng Huang, Chuwen Xue, Tiehan Cao and Katsuhiko Suzuki
Int. J. Mol. Sci. 2025, 26(9), 4126; https://doi.org/10.3390/ijms26094126 - 26 Apr 2025
Viewed by 301
Abstract
Medium-chain fatty acids (MCFAs) refer to a mixture of fatty acids typically composed of 6 to 12 carbon atoms. The unique transport and rapid metabolism of MCFAs provide more clinical benefits than other substrates, such as long-chain fatty acids. Although many studies have [...] Read more.
Medium-chain fatty acids (MCFAs) refer to a mixture of fatty acids typically composed of 6 to 12 carbon atoms. The unique transport and rapid metabolism of MCFAs provide more clinical benefits than other substrates, such as long-chain fatty acids. Although many studies have shown that MCFAs may improve exercise capacity and muscle strength, applications have mainly been limited to low doses. This study explores the effects of high-dose MCFA intake on muscle strength and exercise endurance. Mice were fed high-fat diets containing 30, 35, and 40% (w/w) MCFAs for 12 weeks, and measurements of grip strength and submaximal endurance exercise capacity were conducted to evaluate muscle function. Results showed that compared to the 30% MCFAs group, the absolute grip strength in the 35 and 40% MCFAs groups significantly increased; in terms of endurance performance, the 35% MCFAs group showed a significant increase compared to the 40% MCFAs group. These results were mainly achieved by promoting muscle regeneration and differentiation and inhibiting the expression of the ubiquitin-proteasome pathway. This study demonstrates that moderately increasing MCFA intake can improve the effects of obesity-induced muscle atrophy. However, excessive intake may reduce the impact of improvement. Full article
(This article belongs to the Special Issue Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies)
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17 pages, 1899 KiB  
Article
Luteolin Induces Nrf2 Activity in C2C12 Cells: Implications for Muscle Health
by Nicole Böttcher, Frank Suhr, Thomas Pufe, Christoph Jan Wruck and Athanassios Fragoulis
Int. J. Mol. Sci. 2025, 26(9), 4092; https://doi.org/10.3390/ijms26094092 - 25 Apr 2025
Viewed by 282
Abstract
Chronic oxidative distress results in cellular damage, necessitating adaptive mechanisms for redox balance. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is pivotal in the regulation of key antioxidant and cytoprotective genes. Under normal conditions, Nrf2 undergoes rapid degradation through polyubiquitination. [...] Read more.
Chronic oxidative distress results in cellular damage, necessitating adaptive mechanisms for redox balance. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is pivotal in the regulation of key antioxidant and cytoprotective genes. Under normal conditions, Nrf2 undergoes rapid degradation through polyubiquitination. However, it can be activated during oxidative eustress and distress via modifications of its inhibitor Kelch-like ECH-associated protein 1 (KEAP1). Activation of the Nrf2-Keap1 signaling pathway may decelerate aging-related muscle degeneration, such as sarcopenia and cachexia. In this study, we investigated the efficacy of two muscle-active endogenous factors, creatine and L-β-aminoisobutyric acid (L-BAIBA), as well as two natural phytochemicals, luteolin and silibinin, to induce Nrf2 in the murine myoblast cell line C2C12. Our results revealed that only luteolin significantly enhances Nrf2 activity in both proliferating and differentiated C2C12 cells, leading to increased expression of Nrf2 target genes in proliferating C2C12 cells. In contrast, the other three compounds had either no or only minor effects on Nrf2 activity or target gene expression. Our results underscore the distinct responses of C2C12 cells to different Nrf2 activators, emphasizing the significance of cellular context in their biological effects and highlight luteolin as a potential future treatment option to counteract muscle wasting associated with sarcopenia and cachexia. Full article
(This article belongs to the Special Issue Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies)
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13 pages, 283 KiB  
Article
Might Thyroid Function in Patients with Turner Syndrome Have a Significant Impact on Their Muscle Strength?
by Mariola Krzyscin, Elżbieta Sowińska-Przepiera, Žana Bumbulienė and Anhelli Syrenicz
Int. J. Mol. Sci. 2025, 26(8), 3679; https://doi.org/10.3390/ijms26083679 - 13 Apr 2025
Viewed by 390
Abstract
Turner syndrome (TS) is a genetic disorder caused by abnormalities in one of the X chromosomes. Individuals with TS have a higher incidence of autoimmune thyroid disorders, particularly Hashimoto’s disease, leading to thyroid dysfunction, most commonly hypothyroidism. Hormonal imbalance, growth hormone deficiency, and [...] Read more.
Turner syndrome (TS) is a genetic disorder caused by abnormalities in one of the X chromosomes. Individuals with TS have a higher incidence of autoimmune thyroid disorders, particularly Hashimoto’s disease, leading to thyroid dysfunction, most commonly hypothyroidism. Hormonal imbalance, growth hormone deficiency, and reduced physical activity contribute to muscle weakness in TS patients, and thyroid dysfunction can exacerbate these effects. The purpose of this study was to evaluate whether thyroid factors affect muscle strength in female patients with TS. The study included 70 women with TS and 88 age- and weight-matched controls. TS diagnoses were genetically confirmed (mosaic karyotypes: n = 20; monosomy X: n = 37; structural abnormalities: n = 7). The main criterion for exclusion from the study was unbalanced thyroid function. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and thyroid antibodies (anti-thyroid peroxidase antibodies (aTPO), anti-thyroglobulin antibodies (aTG)) were measured, and muscle strength was assessed using hand-held dynamometry. In TS patients, higher TSH levels were positively correlated, and higher fT4 levels were negatively correlated with muscle strength. No such correlations were found in controls. Thyroid compensation may impact musculoskeletal health in TS. Lower-normal TSH levels are associated with reduced muscle strength, and autoimmune thyroid changes like aTPO and aTG may contribute to muscle deterioration. Further research is needed to confirm these findings. Full article
(This article belongs to the Special Issue Skeletal Muscle Metabolism—Effects of Diet, Exercise and Pharmacotherapies)
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