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Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 9447

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Special Issue Editor

Dr. Andrea Telek

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Guest Editor

Department of Physiology, University of Debrecen, Debrecen, Hungary
Interests: skeletal muscle

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the most recent findings about molecular advances in skeletal muscle function. Despite the recent improvements in this field, important information is still missing about skeletal muscle metabolism. Mitochondria serve as the final targets of metabolism-related signalization pathways and their dynamic nature requires precise regulatory mechanisms. A final response could be modified by epigenetic mechanisms including the inhibition of protein translation by miRNA and other forms of gene expression regulation. Since skeletal muscle is involved in lipid and glucose homeostasis, it can serve as a target in the treatment of metabolic disorders. Additionally, understanding the molecular background of disorders primarily affecting skeletal muscle could improve therapeutic options in dystrophies, age-related muscle atrophy, and sarcopenia. Regarded together, further research needs to be performed to completely understand the molecular regulation of skeletal muscle function. Therefore, we kindly invite you to publish your results in this Special Issue of IJMS entitled “Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment”. Original research papers as well as reviews are encouraged.

Dr. Andrea Telek
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

skeletal muscle
metabolism
mitochondria
epigenetics
exercise
signalization

Published Papers (6 papers)

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Research

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15 pages, 1990 KiB

Open AccessArticle

Investigating the Effects of Diet-Induced Prediabetes on Skeletal Muscle Strength in Male Sprague Dawley Rats

by Mandlakazi Dlamini and Andile Khathi

Int. J. Mol. Sci. 2024, 25(7), 4076; https://doi.org/10.3390/ijms25074076 - 06 Apr 2024

Viewed by 517

Abstract

Type 2 diabetes mellitus, a condition preceded by prediabetes, is documented to compromise skeletal muscle health, consequently affecting skeletal muscle structure, strength, and glucose homeostasis. A disturbance in skeletal muscle functional capacity has been demonstrated to induce insulin resistance and hyperglycemia. However, the modifications in skeletal muscle function in the prediabetic state are not well elucidated. Hence, this study investigated the effects of diet-induced prediabetes on skeletal muscle strength in a prediabetic model. Male Sprague Dawley rats were randomly assigned to one of the two groups (n = 6 per group; six prediabetic (PD) and six non-pre-diabetic (NPD)). The PD group (n = 6) was induced with prediabetes for 20 weeks. The diet that was used to induce prediabetes consisted of fats (30% Kcal/g), proteins (15% Kcal/g), and carbohydrates (55% Kcal/g). In addition to the diet, the experimental animals (n = 6) were supplied with drinking water that was supplemented with 15% fructose. The control group (n = 6) was allowed access to normal rat chow, consisting of 35% carbohydrates, 30% protein, 15% fats, and 20% other components, as well as ordinary tap water. At the end of week 20, the experimental animals were diagnosed with prediabetes using the American Diabetes Association (ADA) prediabetes impaired fasting blood glucose criteria (5.6–6.9 mmol/L). Upon prediabetes diagnosis, the animals were subjected to a four-limb grip strength test to assess skeletal muscle strength at week 20. After the grip strength test was conducted, the animals were euthanized for blood and tissue collection to analyze glycated hemoglobin (HbA1c), plasma insulin, and insulin resistance using the homeostatic model of insulin resistance (HOMA-IR) index and malondialdehyde (MDA) concentration. Correlation analysis was performed to examine the associations of skeletal muscle strength with HOMA-IR, plasma glucose, HbA1c, and MDA concentration. The results demonstrated increased HbA1c, FBG, insulin, HOMA-IR, and MDA concentrations in the PD group compared to the NPD group. Grip strength was reduced in the PD group compared to the NPD group. Grip strength was negatively correlated with HbA1c, plasma glucose, HOMA-IR, and MDA concentration in the PD group. These observations suggest that diet-induced prediabetes compromises muscle function, which may contribute to increased levels of sedentary behavior during prediabetes progression, and this may contribute to the development of hyperglycemia in T2DM. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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16 pages, 2911 KiB

Open AccessArticle

Functional and Morphological Differences of Muscle Mitochondria in Chronic Fatigue Syndrome and Post-COVID Syndrome

by Daniel Alexander Bizjak, Birgit Ohmayer, Jasmine Leonike Buhl, Elisabeth Marion Schneider, Paul Walther, Enrico Calzia, Achim Jerg, Lynn Matits and Jürgen Michael Steinacker

Int. J. Mol. Sci. 2024, 25(3), 1675; https://doi.org/10.3390/ijms25031675 - 30 Jan 2024

Cited by 3 | Viewed by 4492

Abstract

Patients suffering from chronic fatigue syndrome (CFS) or post-COVID syndrome (PCS) exhibit a reduced physiological performance capability. Impaired mitochondrial function and morphology may play a pivotal role. Thus, we aimed to measure the muscle mitochondrial oxidative phosphorylation (OXPHOS) capacity and assess mitochondrial morphology in CFS and PCS patients in comparison to healthy controls (HCs). Mitochondrial OXPHOS capacity was measured in permeabilized muscle fibers using high-resolution respirometry. Mitochondrial morphology (subsarcolemmal/intermyofibrillar mitochondrial form/cristae/diameter/circumference/area) and content (number and proportion/cell) were assessed via electron microscopy. Analyses included differences in OXPHOS between HC, CFS, and PCS, whereas comparisons in morphology/content were made for CFS vs. PCS. OXPHOS capacity of complex I, which was reduced in PCS compared to HC. While the subsarcolemmal area, volume/cell, diameter, and perimeter were higher in PCS vs. CFS, no difference was observed for these variables in intermyofibrillar mitochondria. Both the intermyofibrillar and subsarcolemmal cristae integrity was higher in PCS compared to CFS. Both CFS and PCS exhibit increased fatigue and impaired mitochondrial function, but the progressed pathological morphological changes in CFS suggest structural changes due to prolonged inactivity or unknown molecular causes. Instead, the significantly lower complex I activity in PCS suggests probably direct virus-induced alterations. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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16 pages, 2503 KiB

Open AccessArticle

A Novel Role for DOC2B in Ameliorating Palmitate-Induced Glucose Uptake Dysfunction in Skeletal Muscle Cells via a Mechanism Involving β-AR Agonism and Cofilin

by Jinhee Hwang, Rekha Balakrishnan, Eunjin Oh, Rajakrishnan Veluthakal and Debbie C. Thurmond

Int. J. Mol. Sci. 2024, 25(1), 137; https://doi.org/10.3390/ijms25010137 - 21 Dec 2023

Cited by 1 | Viewed by 825

Abstract

Diet-related lipotoxic stress is a significant driver of skeletal muscle insulin resistance (IR) and type 2 diabetes (T2D) onset. β₂-adrenergic receptor (β-AR) agonism promotes insulin sensitivity in vivo under lipotoxic stress conditions. Here, we established an in vitro paradigm of lipotoxic stress using palmitate (Palm) in rat skeletal muscle cells to determine if β-AR agonism could cooperate with double C-2-like domain beta (DOC2B) enrichment to promote skeletal muscle insulin sensitivity under Palm-stress conditions. Previously, human T2D skeletal muscles were shown to be deficient for DOC2B, and DOC2B enrichment resisted IR in vivo. Our Palm-stress paradigm induced IR and β-AR resistance, reduced DOC2B protein levels, triggered cytoskeletal cofilin phosphorylation, and reduced GLUT4 translocation to the plasma membrane (PM). By enhancing DOC2B levels in rat skeletal muscle, we showed that the deleterious effects of palmitate exposure upon cofilin, insulin, and β-AR-stimulated GLUT4 trafficking to the PM and glucose uptake were preventable. In conclusion, we revealed a useful in vitro paradigm of Palm-induced stress to test for factors that can prevent/reverse skeletal muscle dysfunctions related to obesity/pre-T2D. Discerning strategies to enrich DOC2B and promote β-AR agonism can resist skeletal muscle IR and halt progression to T2D. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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13 pages, 3106 KiB

Open AccessArticle

Circulating Levels of IL-8 and MCP-1 in Healthy Adults: Changes after an Acute Aerobic Exercise and Association with Body Composition and Energy Metabolism

by Rudite Lagzdina, Maija Rumaka, Gita Gersone and Peteris Tretjakovs

Int. J. Mol. Sci. 2023, 24(19), 14725; https://doi.org/10.3390/ijms241914725 - 29 Sep 2023

Viewed by 693

Abstract

The most recent WHO recommendations about physical activity emphasise the importance of total exercise volume above the significance of the duration of each bout. This study examined whether acute aerobic exercise changes circulating levels of IL-8 and MCP-1 and if these changes are associated with body composition and energy metabolism. Healthy adult volunteers completed a 10 min walking–running exercise on a treadmill. Indirect calorimetry was used to determine their resting metabolic rate (RMR) and energy expenditure (EE) during the exercise. Pre-exercise levels of IL-8 and MCP-1 were similar in both sexes. There were positive correlations of pre-exercise IL-8 with body mass, waist circumference, and lean body mass in men and pre-exercise MCP-1 with RMR in women. The exercise led to an increase in IL-8 of 68% and a decrease in MCP-1 of 74% of participants. An increase in post-exercise IL-8 in men was associated with greater walking EE and a greater increase in walking EE. The increase in post-exercise MCP-1 was associated with a lower RMR and running EE in women. There are both sex and individual variations in changes in chemokine secretion in response to the same exercise situation and their associations with values of metabolic parameters. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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25 pages, 5032 KiB

Open AccessArticle

Reciprocal Regulation of Peroxisome Biogenesis and Myogenic Factors Is Critical for Myogenesis

by Chuan-Che Wu, Wei-Cheng Chen, Wen-Po Hsiao, Kai-Fan Huang, Yi-Shiuan Liao, Huang-Bin Lin, Yi-Ju Wu, Chien-Han Kao and Shen-Liang Chen

Int. J. Mol. Sci. 2023, 24(15), 12262; https://doi.org/10.3390/ijms241512262 - 31 Jul 2023

Cited by 2 | Viewed by 1002

Abstract

Mitochondria (MITO) and peroxisomes (PEXO) are the major organelles involved in the oxidative metabolism of cells, but detailed examination of their dynamics and functional adaptations during skeletal muscle (SKM) development (myogenesis) is still lacking. In this study, we found that during myogenesis, MITO DNA, ROS level, and redox ratio increased in myotubes, but the membrane potential (Δψm) and ATP content reduced, implying that the MITO efficiency might reduce during myogenesis. The PEXO number and density both increased during myogenesis, which probably resulted from the accumulation and increased biogenesis of PEXO. The expression of PEXO biogenesis factors was induced during myogenesis in vitro and in utero, and their promoters were also activated by MyoD. Knockdown of the biogenesis factors Pex3 repressed not only the PEXO density and functions but also the levels of MITO genes and functions, suggesting a close coupling between PEXO biogenesis and MITO functions. Surprisingly, Pex3 knockdown by the CRISPRi system repressed myogenic differentiation, indicating critical involvement of PEXO biogenesis in myogenesis. Taken together, these observations suggest that the dynamics and functions of both MITO and PEXO are coupled with each other and with the metabolic changes that occur during myogenesis, and these metabolic couplings are critical to myogenesis. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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Review

Jump to: Research

20 pages, 2419 KiB

Open AccessReview

Prediabetes-Associated Changes in Skeletal Muscle Function and Their Possible Links with Diabetes: A Literature Review

by Mandlakazi Dlamini and Andile Khathi

Int. J. Mol. Sci. 2024, 25(1), 469; https://doi.org/10.3390/ijms25010469 - 29 Dec 2023

Viewed by 1110

Abstract

The skeletal muscle plays a critical role in regulating systemic blood glucose homeostasis. Impaired skeletal muscle glucose homeostasis associated with type 2 diabetes mellitus (T2DM) has been observed to significantly affect the whole-body glucose homeostasis, thereby resulting in other diabetic complications. T2DM does not only affect skeletal muscle glucose homeostasis, but it also affects skeletal muscle structure and functional capacity. Given that T2DM is a global health burden, there is an urgent need to develop therapeutic medical therapies that will aid in the management of T2DM. Prediabetes (PreDM) is a prominent risk factor of T2DM that usually goes unnoticed in many individuals as it is an asymptomatic condition. Hence, research on PreDM is essential because establishing diabetic biomarkers during the prediabetic state would aid in preventing the development of T2DM, as PreDM is a reversible condition if it is detected in the early stages. The literature predominantly documents the changes in skeletal muscle during T2DM, but the changes in skeletal muscle during prediabetes are not well elucidated. In this review, we seek to review the existing literature on PreDM- and T2DM-associated changes in skeletal muscle function. Full article

(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment)

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