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Skeletal Muscle and Metabolic Disorders
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Skeletal Muscle and Metabolic Disorders

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 (25 October 2022) | Viewed by 8419

Special Issue Editors

Dr. Sibhghatulla Shaikh

E-Mail Website
Guest Editor
Department of Medical Biotechnology, Yeungnam University, Gyeongsan 38541, Korea
Interests: Skeletal muscle; Metabolic disorders; Sarcopenia; Drug designing; Diabetes; Natural compounds
Dr. Tatiana Kostrominova

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, Indiana University School of Medicine-Northwest, 3400 Broadway St., Gary, IN 46408-1197, USA
Interests: skeletal muscle; tendon; aging; muscle denervation; muscle unloading; obesity; myokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle, the largest organ in the body, mainly provides mobility, protects and maintains the skeleton, and controls the body’s temperature and glucose homeostasis. It is the core metabolic tissue of the glucose homeostasis regulator and is responsible for approximately 80% of postprandial glucose uptake from the blood circulation. Skeletal muscle is crucial for metabolism, both because of its role in glucose uptake and its importance in exercise and metabolic disorders. In addition, skeletal muscle is recognized as an endocrine and paracrine organ. Muscle-derived secretive proteins, known as myokines, mediate the connections between skeletal muscle mass and other tissues, such as the liver, adipose tissue, pancreas, bone, and cardiovascular system. Decreased levels of physical activity and skeletal muscle loss (sarcopenia) are associated with physical fatigue and impairment during aging, leading to several metabolic diseases.

This Special Issue will highlight new research broadly on metabolic disorder associated with skeletal muscle using state-of-the-art techniques. Original research papers and reviews on these and related topics are welcome.

Dr. Sibhghatulla Shaikh
Dr. Tatiana Kostrominova
Guest Editors

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
  • Metabolic disorders
  • Sarcopenia
  • Drug design
  • Diabetes
  • Natural compounds
  • Insulin resistance
  • Glucose metabolism

Published Papers (4 papers)

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Research

20 pages, 7304 KiB  
Article
Coapplication of Magnesium Supplementation and Vibration Modulate Macrophage Polarization to Attenuate Sarcopenic Muscle Atrophy through PI3K/Akt/mTOR Signaling Pathway
by Can Cui, Zhengyuan Bao, Simon Kwoon-Ho Chow, Ronald Man Yeung Wong, Ailsa Welch, Ling Qin and Wing Hoi Cheung
Int. J. Mol. Sci. 2022, 23(21), 12944; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112944 - 26 Oct 2022
Cited by 4 | Viewed by 2376
Abstract
Sarcopenia is an age-related geriatric syndrome characterized by the gradual loss of muscle mass and function. Low-magnitude high-frequency vibration (LMHFV) was shown to be beneficial to structural and functional outcomes of skeletal muscles, while magnesium (Mg) is a cofactor associated with better indices [...] Read more.
Sarcopenia is an age-related geriatric syndrome characterized by the gradual loss of muscle mass and function. Low-magnitude high-frequency vibration (LMHFV) was shown to be beneficial to structural and functional outcomes of skeletal muscles, while magnesium (Mg) is a cofactor associated with better indices of skeletal muscle mass and strength. We hypothesized that LMHFV, Mg and their combinations could suppress inflammation and sarcopenic atrophy, promote myogenesis via PI3k/Akt/mTOR pathway in senescence-accelerated mouse P8 (SAMP8) mice and C2C12 myoblasts. Results showed that Mg treatment and LMHFV could significantly decrease inflammatory expression (C/EBPα and LYVE1) and modulate a CD206-positive M2 macrophage population at month four. Mg treatment also showed significant inhibitory effects on FOXO3, MuRF1 and MAFbx mRNA expression. Coapplication showed a synergistic effect on suppression of type I fiber atrophy, with significantly higher IGF-1, MyoD, MyoG mRNA (p < 0.05) and pAkt protein expression (p < 0.0001) during sarcopenia. In vitro inhibition of PI3K/Akt and mTOR abolished the enhancement effects on myotube formation and inhibited MRF mRNA and p85, Akt, pAkt and mTOR protein expressions. The present study demonstrated that the PI3K/Akt/mTOR pathway is the predominant regulatory mechanism through which LMHFV and Mg enhanced muscle regeneration and suppressed atrogene upregulation. Full article
(This article belongs to the Special Issue Skeletal Muscle and Metabolic Disorders)
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12 pages, 3265 KiB  
Article
Elemental Composition of Skeletal Muscle Fibres Studied with Synchrotron Radiation X-ray Fluorescence (SR-XRF)
by Paula Kasprzyk, Paweł M. Wróbel, Joanna Dudała, Kalotina Geraki, Magdalena Szczerbowska-Boruchowska, Edyta Radwańska, Roger M. Krzyżewski, Dariusz Adamek and Marek Lankosz
Int. J. Mol. Sci. 2022, 23(14), 7931; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23147931 - 19 Jul 2022
Cited by 1 | Viewed by 1205
Abstract
Diseases of the muscle tissue, particularly those disorders which result from the pathology of individual muscle cells, are often called myopathies. The diversity of the content of individual cells is of interest with regard to their role in both biochemical mechanisms and the [...] Read more.
Diseases of the muscle tissue, particularly those disorders which result from the pathology of individual muscle cells, are often called myopathies. The diversity of the content of individual cells is of interest with regard to their role in both biochemical mechanisms and the structure of muscle tissue itself. These studies focus on the preliminary analysis of the differences that may occur between diseased tissues and tissues that have been recognised as a reference group. To do so, 13 samples of biopsied human muscle tissues were studied: 3 diagnosed as dystrophies, 6 as (non-dystrophic) myopathy and 4 regarded as references. From these sets of muscle biopsies, 135 completely measured muscle fibres were separated altogether, which were subjected to investigations using synchrotron radiation X-ray fluorescence (SR-XRF). Muscle fibres were analysed in terms of the composition of elements such as Br, Ca, Cl, Cr, Cu, Fe, K, Mn, P, S and Zn. The performed statistical tests indicate that all three groups (dystrophies—D; myopathies—M; references—R) show statistically significant differences in their elemental compositions, and the greatest impact, according to the multivariate discriminate analysis (MDA), comes from elements such as Ca, Cu, K, Cl and S. Full article
(This article belongs to the Special Issue Skeletal Muscle and Metabolic Disorders)
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18 pages, 4632 KiB  
Article
Enhanced Muscle Strength in Dyslipidemic Mice and Its Relation to Increased Capacity for Fatty Acid Oxidation
by Marta Tomczyk, Alicja Braczko, Patrycja Jablonska, Adriana Mika, Kamil Przyborowski, Agata Jedrzejewska, Oliwia Krol, Filip Kus, Tomasz Sledzinski, Stefan Chlopicki, Ewa M. Slominska and Ryszard T. Smolenski
Int. J. Mol. Sci. 2021, 22(22), 12251; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212251 - 12 Nov 2021
Cited by 2 | Viewed by 2119
Abstract
Dyslipidemia is commonly linked to skeletal muscle dysfunction, accumulation of intramyocellular lipids, and insulin resistance. However, our previous research indicated that dyslipidemia in apolipoprotein E and low-density lipoprotein receptor double knock-out mice (ApoE/LDLR -/-) leads to improvement of exercise capacity. This study aimed [...] Read more.
Dyslipidemia is commonly linked to skeletal muscle dysfunction, accumulation of intramyocellular lipids, and insulin resistance. However, our previous research indicated that dyslipidemia in apolipoprotein E and low-density lipoprotein receptor double knock-out mice (ApoE/LDLR -/-) leads to improvement of exercise capacity. This study aimed to investigate in detail skeletal muscle function and metabolism in these dyslipidemic mice. We found that ApoE/LDLR -/- mice showed an increased grip strength as well as increased troponins, and Mhc2 levels in skeletal muscle. It was accompanied by the increased skeletal muscle mitochondria numbers (judged by increased citrate synthase activity) and elevated total adenine nucleotides pool. We noted increased triglycerides contents in skeletal muscles and increased serum free fatty acids (FFA) levels in ApoE/LDLR -/- mice. Importantly, Ranolazine mediated inhibition of FFA oxidation in ApoE/LDLR -/- mice led to the reduction of exercise capacity and total adenine nucleotides pool. Thus, this study demonstrated that increased capacity for fatty acid oxidation, an adaptive response to dyslipidemia leads to improved cellular energetics that translates to increased skeletal muscle strength and contributes to increased exercise capacity in ApoE/LDLR -/- mice. Full article
(This article belongs to the Special Issue Skeletal Muscle and Metabolic Disorders)
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10 pages, 3398 KiB  
Article
Double p52Shc/p46Shc Rat Knockout Demonstrates Severe Gait Abnormalities Accompanied by Dilated Cardiomyopathy
by Bradley Miller, Tatiana Y. Kostrominova, Aron M. Geurts and Andrey Sorokin
Int. J. Mol. Sci. 2021, 22(10), 5237; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105237 - 15 May 2021
Cited by 1 | Viewed by 1668
Abstract
The ubiquitously expressed adaptor protein Shc exists in three isoforms p46Shc, p52Shc, and p66Shc, which execute distinctly different actions in cells. The role of p46Shc is insufficiently studied, and the purpose of this study was to further investigate its functional significance. We developed [...] Read more.
The ubiquitously expressed adaptor protein Shc exists in three isoforms p46Shc, p52Shc, and p66Shc, which execute distinctly different actions in cells. The role of p46Shc is insufficiently studied, and the purpose of this study was to further investigate its functional significance. We developed unique rat mutants lacking p52Shc and p46Shc isoforms (p52Shc/46Shc-KO) and carried out histological analysis of skeletal and cardiac muscle of parental and genetically modified rats with impaired gait. p52Shc/46Shc-KO rats demonstrate severe functional abnormalities associated with impaired gait. Our analysis of p52Shc/46Shc-KO rat axons and myelin sheets in cross-sections of the sciatic nerve revealed the presence of significant anomalies. Based on the lack of skeletal muscle fiber atrophy and the presence of sciatic nerve abnormalities, we suggest that the impaired gait in p52Shc/46Shc-KO rats might be due to the sensory feedback from active muscle to the brain locomotor centers. The lack of dystrophin in some heart muscle fibers reflects damage due to dilated cardiomyopathy. Since rats with only p52Shc knockout do not display the phenotype of p52Shc/p46Shc-KO, abnormal locomotion is likely to be caused by p46Shc deletion. Our data suggest a previously unknown role of 46Shc actions and signaling in regulation of gait. Full article
(This article belongs to the Special Issue Skeletal Muscle and Metabolic Disorders)
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