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Sarcopenic Obesity: Mechanisms and Countermeasures
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Sarcopenic Obesity: Mechanisms and Countermeasures

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 (15 June 2021) | Viewed by 21006

Special Issue Editors

Prof. Dr. Giuseppe D'Antona

E-Mail Website
Guest Editor
Department of Public Health, Experimental and Forensic Medicine and CRIAMS-Sport Medicine Centre Voghera, Pavia University, Viale Foscolo 12, 27058 Voghera, Italy
Interests: muscle physiology; muscle physiophatology; exercise physiology; sport nutrition; nutritional supplements
Dr. Massimo Negro

E-Mail Website
Guest Editor
CRIAMS-Sport Medicine Centre Voghera, University of Pavia, Voghera, Italy
Interests: muscle physiology; physiophatology; exercise physiology; sport nutrition

Special Issue Information

Sarcopenic obesity is a chronic condition, characterized by sarcopenia concomitant to fat mass accumulation.

In presence of the disease, subjects usually manifest obesity-related comorbidities (e.g., type 2 diabetes mellitus, dyslipidemia, and hypertension) and/or symptoms related to sarcopenia per se (e.g., weakness, fatigue, and frailty).

Considering that this condition includes factors leading to the simultaneous deterioration of skeletal muscle mass and an increase in fat mass, the common mechanisms capable of acting on muscle and adipose tissue physiology should be taken into account.

This Special Issue will highlight emerging research on the pathogenesis of sarcopenic obesity and on the cornerstones of its management and prevention, with special focus on nutritional and physical approaches.

We welcome different types of manuscript submissions, including original preclinical and clinical research articles and up-to-date reviews (narrative and systematic reviews, as well as meta-analyses).

Dr. Giuseppe D'Antona
Dr. Massimo Negro
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

  • sarcopenia
  • obesity
  • nutritional supplementation
  • nutrition
  • physical activity
  • inflammation

Published Papers (4 papers)

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Review

24 pages, 1334 KiB  
Review
The Role of Sarcopenic Obesity in Cancer and Cardiovascular Disease: A Synthesis of the Evidence on Pathophysiological Aspects and Clinical Implications
by Erika Aparecida Silveira, Rômulo Roosevelt da Silva Filho, Maria Claudia Bernardes Spexoto, Fahimeh Haghighatdoost, Nizal Sarrafzadegan and Cesar de Oliveira
Int. J. Mol. Sci. 2021, 22(9), 4339; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094339 - 21 Apr 2021
Cited by 27 | Viewed by 4265
Abstract
Obesity is globally a serious public health concern and is associated with a high risk of cardiovascular disease (CVD) and various types of cancers. It is important to evaluate various types of obesity, such as visceral and sarcopenic obesity. The evidence on the [...] Read more.
Obesity is globally a serious public health concern and is associated with a high risk of cardiovascular disease (CVD) and various types of cancers. It is important to evaluate various types of obesity, such as visceral and sarcopenic obesity. The evidence on the associated risk of CVD, cancer and sarcopenic obesity, including pathophysiological aspects, occurrence, clinical implications and survival, needs further investigation. Sarcopenic obesity is a relatively new term. It is a clinical condition that primarily affects older adults. There are several endocrine-hormonal, metabolic and lifestyle aspects involved in the occurrence of sarcopenic obesity that affect pathophysiological aspects that, in turn, contribute to CVD and neoplasms. However, there is no available evidence on the role of sarcopenic obesity in the occurrence of CVD and cancer and its pathophysiological interplay. Therefore, this review aims to describe the pathophysiological aspects and the clinical and epidemiological evidence on the role of sarcopenic obesity related to the occurrence and mortality risk of various types of cancer and cardiovascular disease. This literature review highlights the need for further research on sarcopenic obesity to demonstrate the interrelation of these various associations. Full article
(This article belongs to the Special Issue Sarcopenic Obesity: Mechanisms and Countermeasures)
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33 pages, 789 KiB  
Review
An Overview of the Molecular Mechanisms Contributing to Musculoskeletal Disorders in Chronic Liver Disease: Osteoporosis, Sarcopenia, and Osteoporotic Sarcopenia
by Young Joo Yang and Dong Joon Kim
Int. J. Mol. Sci. 2021, 22(5), 2604; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052604 - 05 Mar 2021
Cited by 49 | Viewed by 6304
Abstract
The prevalence of osteoporosis and sarcopenia is significantly higher in patients with liver disease than in those without liver disease and osteoporosis and sarcopenia negatively influence morbidity and mortality in liver disease, yet these musculoskeletal disorders are frequently overlooked in clinical practice for [...] Read more.
The prevalence of osteoporosis and sarcopenia is significantly higher in patients with liver disease than in those without liver disease and osteoporosis and sarcopenia negatively influence morbidity and mortality in liver disease, yet these musculoskeletal disorders are frequently overlooked in clinical practice for patients with chronic liver disease. The objective of this review is to provide a comprehensive understanding of the molecular mechanisms of musculoskeletal disorders accompanying the pathogenesis of liver disease. The increased bone resorption through the receptor activator of nuclear factor kappa (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) system and upregulation of inflammatory cytokines and decreased bone formation through increased bilirubin and sclerostin and lower insulin-like growth factor-1 are important mechanisms for osteoporosis in patients with liver disease. Sarcopenia is associated with insulin resistance and obesity in non-alcoholic fatty liver disease, whereas hyperammonemia, low amount of branched chain amino acids, and hypogonadism contributes to sarcopenia in liver cirrhosis. The bidirectional crosstalk between muscle and bone through myostatin, irisin, β-aminoisobutyric acid (BAIBA), osteocalcin, as well as the activation of the RANK and the Wnt/β-catenin pathways are associated with osteosarcopenia. The increased understandings for these musculoskeletal disorders would be contributes to the development of effective therapies targeting the pathophysiological mechanism involved. Full article
(This article belongs to the Special Issue Sarcopenic Obesity: Mechanisms and Countermeasures)
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13 pages, 348 KiB  
Review
Sarcopenic Obesity in Liver Cirrhosis: Possible Mechanism and Clinical Impact
by Hiroki Nishikawa, Hirayuki Enomoto, Shuhei Nishiguchi and Hiroko Iijima
Int. J. Mol. Sci. 2021, 22(4), 1917; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041917 - 15 Feb 2021
Cited by 32 | Viewed by 4183
Abstract
The picture of chronic liver diseases (CLDs) has changed considerably in recent years. One of them is the increase of non-alcoholic fatty liver disease. More and more CLD patients, even those with liver cirrhosis (LC), tend to be presenting with obesity these days. [...] Read more.
The picture of chronic liver diseases (CLDs) has changed considerably in recent years. One of them is the increase of non-alcoholic fatty liver disease. More and more CLD patients, even those with liver cirrhosis (LC), tend to be presenting with obesity these days. The annual rate of muscle loss increases with worsening liver reserve, and thus LC patients are more likely to complicate with sarcopenia. LC is also characterized by protein-energy malnutrition (PEM). Since the PEM in LC can be invariable, the patients probably present with sarcopenic obesity (Sa-O), which involves both sarcopenia and obesity. Currently, there is no mention of Sa-O in the guidelines; however, the rapidly increasing prevalence and poorer clinical consequences of Sa-O are recognized as an important public health problem, and the diagnostic value of Sa-O is expected to increase in the future. Sa-O involves a complex interplay of physiological mechanisms, including increased inflammatory cytokines, oxidative stress, insulin resistance, hormonal disorders, and decline of physical activity. The pathogenesis of Sa-O in LC is diverse, with a lot of perturbations in the muscle–liver–adipose tissue axis. Here, we overview the current knowledge of Sa-O, especially focusing on LC. Full article
(This article belongs to the Special Issue Sarcopenic Obesity: Mechanisms and Countermeasures)
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21 pages, 2166 KiB  
Review
Dysregulated Autophagy Mediates Sarcopenic Obesity and Its Complications via AMPK and PGC1α Signaling Pathways: Potential Involvement of Gut Dysbiosis as a Pathological Link
by Ji Yeon Ryu, Hyung Muk Choi, Hyung-In Yang and Kyoung Soo Kim
Int. J. Mol. Sci. 2020, 21(18), 6887; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186887 - 19 Sep 2020
Cited by 20 | Viewed by 5475
Abstract
Sarcopenic obesity (SOB), which is closely related to being elderly as a feature of aging, is recently gaining attention because it is associated with many other age-related diseases that present as altered intercellular communication, dysregulated nutrient sensing, and mitochondrial dysfunction. Along with insulin [...] Read more.
Sarcopenic obesity (SOB), which is closely related to being elderly as a feature of aging, is recently gaining attention because it is associated with many other age-related diseases that present as altered intercellular communication, dysregulated nutrient sensing, and mitochondrial dysfunction. Along with insulin resistance and inflammation as the core pathogenesis of SOB, autophagy has recently gained attention as a significant mechanism of muscle aging in SOB. Known as important cellular metabolic regulators, the AMP-activated protein kinase (AMPK) and the peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α) signaling pathways play an important role in autophagy, inflammation, and insulin resistance, as well as mutual communication between skeletal muscle, adipose tissue, and the liver. Furthermore, AMPK and PGC-1α signaling pathways are implicated in the gut microbiome–muscle axis. In this review, we describe the pathological link between SOB and its associated complications such as metabolic, cardiovascular, and liver disease, falls and fractures, osteoarthritis, pulmonary disease, and mental health via dysregulated autophagy controlled by AMPK and/or PGC-1α signaling pathways. Here, we propose potential treatments for SOB by modulating autophagy activity and gut dysbiosis based on plausible pathological links. Full article
(This article belongs to the Special Issue Sarcopenic Obesity: Mechanisms and Countermeasures)
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