A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity

Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with im...

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Published inNutrients Vol. 14; no. 9; p. 1975
Main Authors Zou, Yun-Yi, Chen, Zhang-Lin, Sun, Chen-Chen, Yang, Dong, Zhou, Zuo-Qiong, Xiao, Qin, Peng, Xi-Yang, Tang, Chang-Fa
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 09.05.2022
MDPI
Subjects
Antibodies
Atrophy
Danio rerio
Diabetes
Diet
Epoxy resins
Ethanol
High fat diet
Kinases
Liver
Medical research
Metabolic disorders
Metabolic syndrome
Metabolism
Mitochondria
muscle
Muscles
Musculoskeletal system
Obesity
Oxidation
Proteins
Sarcopenia
sarcopenic obesity
Skeletal muscle
Statistical analysis
Swimming
Transmission electron microscopy
Zebrafish
Denmark
Beijing China
United States > US
China
Japan
zebrafish
sarcopenic obesity
mitochondria
high-fat diet
muscle
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Summary:Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear. In this study, we evaluated the effects of a high-fat diet on muscle mitochondrial function in a zebrafish model of sarcopenic obesity (SOB). In SOB zebrafish, a significant decrease in exercise capacity and skeletal muscle fiber cross-sectional area was detected, accompanied by high expression of the atrophy-related markers Atrogin-1 and muscle RING-finger protein-1. Zebrafish with SOB exhibited inhibition of mitochondrial biogenesis and fatty acid oxidation as well as disruption of mitochondrial fusion and fission in atrophic muscle. Thus, our findings showed that muscle atrophy was associated with SOB-induced mitochondrial dysfunction. Overall, these results showed that the SOB zebrafish model established in this study may provide new insights into the development of therapeutic strategies to manage mitochondria-related muscular atrophy.
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ISSN:2072-6643
2072-6643
DOI:10.3390/nu14091975