The Critical Role of Oxidative Stress in Sarcopenic Obesity

Author:

Gonzalez Andrea123ORCID,Simon Felipe245ORCID,Achiardi Oscar6ORCID,Vilos Cristian37ORCID,Cabrera Daniel89ORCID,Cabello-Verrugio Claudio123ORCID

Affiliation:

1. Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile

2. Millennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile

3. Center for the Development of Nanoscience and Nanotechnology (CEDENNA), Universidad de Santiago de Chile, Santiago 8350709, Chile

4. Millennium Nucleus of Ion Channel-Associated Diseases (MiNICAD), Universidad de Chile, Santiago 8370146, Chile

5. Laboratory of Integrative Physiopathology, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile

6. Escuela de Kinesiología, Facultad de Ciencias, Pontificia Universidad Católica de Valparaíso, Valparaíso 2340025, Chile

7. Laboratory of Nanomedicine and Targeted Delivery, Center for Medical Research, School of Medicine, Universidad de Talca, Talca 3460000, Chile

8. Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago 8330077, Chile

9. Facultad de Ciencias Médicas, Universidad Bernardo O Higgins, Santiago 8370993, Chile

Abstract

Sarcopenic obesity (SO) is a combination of obesity and sarcopenia that primarily develops in older people. Patients with SO have high fat mass, low muscle mass, low muscle strength, and low physical function. SO relates to metabolic syndrome and an increased risk of morbimortality. The prevalence of SO varies because of lacking consensus criteria regarding its definition and the methodological difficulty in diagnosing sarcopenia and obesity. SO includes systemic alterations such as insulin resistance, increased proinflammatory cytokines, age-associated hormonal changes, and decreased physical activity at pathophysiological levels. Interestingly, these alterations are influenced by oxidative stress, which is a critical factor in altering muscle function and the generation of metabolic dysfunctions. Thus, oxidative stress in SO alters muscle mass, the signaling pathways that control it, satellite cell functions, and mitochondrial and endoplasmic reticulum activities. Considering this background, our objectives in this review are to describe SO as a highly prevalent condition and look at the role of oxidative stress in SO pathophysiology.

Funder

CEDENNA

Publisher

Hindawi Limited

Subject

Cell Biology,Ageing,General Medicine,Biochemistry

Reference159 articles.

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