A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity
Open accessAbstract
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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Written from the paper’s full text.
TL;DR
A 16-week high-fat diet in adult zebrafish induced sarcopenic obesity, skeletal muscle atrophy, and impaired swimming capacity. These changes were accompanied by suppressed muscle mitochondrial biogenesis, fatty acid oxidation, and abnormal mitochondrial fusion/fission.
Key findings
- HFD-fed zebrafish had higher body weight, no significant body length difference, increased fasting blood glucose and muscle triglyceride, and fatty liver features after 16 weeks on a 24% fat diet versus a 6% fat normal diet.
- Skeletal muscle atrophy occurred: HFD zebrafish showed smaller muscle fiber sizes, more lipid droplets, and significantly increased atrophy markers Atrogin-1 and MuRF1.
- Swimming capacity was impaired: beyond 6.2 BL/s, ND zebrafish had higher swimming capacity and MO2 than HFD zebrafish; HFD zebrafish had decreased exhaustive swimming time, MO2max, Ucrit, and Ucrit-r.
- Muscle mitochondrial dysfunction was observed: lower phospho-AMPK, SIRT1, and PGC1α; downregulated pgc1α, nrf1, tfam, pparab, cpt1a, and ETC subunit genes (sdha, uqcrc2b, cox4il, atp5f); higher DRP1 and lower OPA1/MFN2; and degenerated, enlarged, swollen mitochondria with broken or absent cristae.
Methods
- Adult male AB strain zebrafish, 4 months old, were adapted for 1 week on a 6% fat commercial diet; 90 healthy zebrafish were randomized to normal diet (6% fat) or high-fat diet (24% fat), with three tanks per diet and 15 zebrafish per tank, fed three times daily for 16 weeks.
- Outcomes included body weight/length, blood glucose, muscle triglyceride/cholesterol, catalase and total SOD, liver and muscle histology (H&E, Masson, Oil Red O), transmission electron microscopy, swimming capacity and oxygen consumption via a miniature swimming tunnel respirator, RT-qPCR, and Western blot.
- Statistical analysis used unpaired t-tests with SPSS or GraphPad Prism; data were means ± SD of three independent experiments, with significance at p < 0.05.
Limitations
- The paper states that SOB has complex pathogenesis including lipotoxicity, mitochondrial dysfunction, inflammation, and insulin resistance, and that the current study only unveiled one aspect; further comprehensive studies are needed to investigate detailed mechanisms and assess pharmacological and exercise-based interventions targeting mitochondria.
- Evident from the text: only adult male zebrafish were used, so sex-specific effects are not addressed; the study reports associations rather than direct causal rescue experiments linking mitochondrial dysfunction to atrophy or swimming impairment; most outcome results are described qualitatively without exact effect sizes or numerical values.
Model-written summary. Check it against the paper before relying on it.
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Cites
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Claims the paper makes
0 of 20 cited sources checked · 0 supported · 0 flagged
- Findingown data
HFD-fed zebrafish exhibited higher body weight compared with ND zebrafish.
“zebrafish fed an HFD exhibited higher body weight compared with those in the ND group (Figure 1A)”
Quote in the paperSubstantial claim - Findingown data
As water speed exceeded 6.2 BL/s, ND zebrafish exhibited higher MO2 levels than HFD zebrafish at each testing stage.
“as the water sped up beyond 6.2 BL/s, zebrafish in the ND group exhibited higher swimming capacity and MO2 levels than those in the HFD group at each testing stage.”
Quote in the paperSubstantial claim - Findingown data
No significant differences in body length were observed between HFD and ND zebrafish.
“whereas no significant differences in body length were observed (Figure 1B)”
Quote in the paperNot a substantial claim - Findingown data
As water speed exceeded 6.2 BL/s, ND zebrafish exhibited higher swimming capacity than HFD zebrafish at each testing stage.
“as the water sped up beyond 6.2 BL/s, zebrafish in the ND group exhibited higher swimming capacity and MO2 levels than those in the HFD group at each testing stage.”
Quote in the paperSubstantial claim - Findingown data
Muscle fiber sizes in transverse sections were smaller in the HFD group than in the ND group.
“H&E staining indicated that the muscle fiber sizes of transverse sections in the HFD group were smaller than those in the ND group (Figure 2A,B).”
Quote in the paperSubstantial claim
- Findingown data
Muscle triglyceride content significantly increased in the HFD group.
“Fasting blood glucose and muscle triglyceride contents significantly increased in the HFD group (Figure 1C,D).”
Quote in the paperSubstantial claim - Findingown data
HFD feeding significantly decreased expression of genes related to mitochondrial biogenesis (pgc1α, nrf1, and tfam).
“we detected significant decreases in the expression of genes related to mitochondrial biogenesis (pgc1α, nrf1, and tfam), fatty oxidation (pparab and cpt1a), and electron transport chain (ETC) complex subunits (sdha, uqcrc2b, cox4il, and atp5f; Figure 4C).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish muscle exhibited more lipid droplets than ND zebrafish muscle.
“the muscles of zebrafish in the HFD group exhibited more lipid droplets.”
Quote in the paperNot a substantial claim - Findingown data
HFD zebrafish exhibited slower Ucrit-r compared with ND zebrafish.
“zebrafish in the HFD group exhibited slower Ucrit and Ucrit-r when compared with those in the ND group (Figure 3E,F).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish exhibited slower Ucrit compared with ND zebrafish.
“zebrafish in the HFD group exhibited slower Ucrit and Ucrit-r when compared with those in the ND group (Figure 3E,F).”
Quote in the paperSubstantial claim - Findingown data
Fasting blood glucose significantly increased in the HFD group.
“Fasting blood glucose and muscle triglyceride contents significantly increased in the HFD group (Figure 1C,D).”
Quote in the paperNot a substantial claim - Findingown data
Expression of Atrogin-1 was significantly increased in the HFD group.
“the expression of muscle atrophy markers (Atrogin-1 and MuRF1) was significantly increased in zebrafish in the HFD group (Figure 2C,D).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish exhibited decreased MO2max values compared with ND zebrafish.
“zebrafish in the HFD group exhibited decreased exhaustive swimming times and MO2max values compared with those in the ND group (Figure 3C,D).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish exhibited decreased exhaustive swimming times compared with ND zebrafish.
“zebrafish in the HFD group exhibited decreased exhaustive swimming times and MO2max values compared with those in the ND group (Figure 3C,D).”
Quote in the paperSubstantial claim - Findingown data
HFD-fed zebrafish had lower muscle levels of phospho-AMPK compared with ND zebrafish.
“we observed lower levels of phospho-AMPK, SIRT1, and PGC1α in the muscles of HFD-fed zebrafish compared with those in zebrafish in the ND group (Figure 4A,B).”
Quote in the paperSubstantial claim - Findingown data
HFD-fed zebrafish had lower muscle levels of SIRT1 compared with ND zebrafish.
“we observed lower levels of phospho-AMPK, SIRT1, and PGC1α in the muscles of HFD-fed zebrafish compared with those in zebrafish in the ND group (Figure 4A,B).”
Quote in the paperSubstantial claim - Findingown data
HFD-fed zebrafish had lower muscle levels of PGC1α compared with ND zebrafish.
“we observed lower levels of phospho-AMPK, SIRT1, and PGC1α in the muscles of HFD-fed zebrafish compared with those in zebrafish in the ND group (Figure 4A,B).”
Quote in the paperSubstantial claim - Findingown data
Expression of MuRF1 was significantly increased in the HFD group.
“the expression of muscle atrophy markers (Atrogin-1 and MuRF1) was significantly increased in zebrafish in the HFD group (Figure 2C,D).”
Quote in the paperSubstantial claim - Findingown data
HFD feeding significantly decreased expression of genes related to fatty acid oxidation (pparab and cpt1a).
“we detected significant decreases in the expression of genes related to mitochondrial biogenesis (pgc1α, nrf1, and tfam), fatty oxidation (pparab and cpt1a), and electron transport chain (ETC) complex subunits (sdha, uqcrc2b, cox4il, and atp5f; Figure 4C).”
Quote in the paperSubstantial claim - Findingown data
HFD feeding significantly decreased expression of genes related to electron transport chain complex subunits (sdha, uqcrc2b, cox4il, and atp5f).
“we detected significant decreases in the expression of genes related to mitochondrial biogenesis (pgc1α, nrf1, and tfam), fatty oxidation (pparab and cpt1a), and electron transport chain (ETC) complex subunits (sdha, uqcrc2b, cox4il, and atp5f; Figure 4C).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish skeletal muscles exhibited lower levels of OPA1 compared with ND zebrafish.
“skeletal muscles of zebrafish in the HFD group exhibited higher expression levels of mitochondrial fission-related proteins (e.g., DRP1) and lower levels of mitochondrial fusion-related proteins (e.g., OPA1 and MFN2; Figure 5A,B).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish skeletal muscles exhibited higher expression levels of mitochondrial fission-related proteins (e.g., DRP1) compared with ND zebrafish.
“skeletal muscles of zebrafish in the HFD group exhibited higher expression levels of mitochondrial fission-related proteins (e.g., DRP1) and lower levels of mitochondrial fusion-related proteins (e.g., OPA1 and MFN2; Figure 5A,B).”
Quote in the paperSubstantial claim - Findingown data
HFD zebrafish skeletal muscles exhibited lower levels of MFN2 compared with ND zebrafish.
“skeletal muscles of zebrafish in the HFD group exhibited higher expression levels of mitochondrial fission-related proteins (e.g., DRP1) and lower levels of mitochondrial fusion-related proteins (e.g., OPA1 and MFN2; Figure 5A,B).”
Quote in the paperSubstantial claim - Premisecitation
Long-term high-fat dietary intake can induce myofibrillar protein degradation and myonuclear apoptosis and ultimately lead to sarcopenia.
“Long-term, high-fat dietary intake can induce myofibrillar protein degradation and myonuclear apoptosis and ultimately lead to sarcopenia [7].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [7] Tournadre, 2019, Sarcopenia, Jt. Bone Spine source
Not checked in the free run.
- Interpretationown data
Swimming capacity of HFD-fed zebrafish was impaired.
“These results indicated that the swimming capacity of HFD-fed zebrafish was impaired.”
Quote in the paperSubstantial claim - Interpretationown data
HFD feeding induced or contributed to obesity in zebrafish.
“These data indicate the successful establishment of HFD-induced obesity in zebrafish.”
- Also stated in: § 4. Discussion · plain
“The current findings further confirmed that long-term HFD feeding contributed to obesity in zebrafish.”
Quote in the paperSubstantial claim - Also stated in: § 4. Discussion · plain
- Premisecitation
Dysregulation of mitochondrial function can accelerate lipid deposition and oxidative stress in muscle, thereby exacerbating the decrease in muscle mass.
“Additionally, the dysregulation of mitochondrial function can accelerate lipid deposition and oxidative stress in muscle, thereby exacerbating the decrease in muscle mass [12].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [12] Genders, A.J., Holloway, G.P., and Bishop, D.J. (2020). Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?. Int. J. Mol. Sci., 21. source
Not checked in the free run.
- Interpretationown data
Long-term HFD feeding caused muscular atrophy in zebrafish.
“These results demonstrated that long-term HFD feeding caused muscular atrophy in zebrafish.”
Quote in the paperSubstantial claim - Premisecitation
Abnormal mitochondrial fusion and fission are responsible for the impairment of mitochondrial function.
“Abnormal mitochondrial fusion and fission are responsible for the impairment of mitochondrial function [16].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [16] Youle, 2012, Mitochondrial fission, fusion, and stress, Science source
Not checked in the free run.
- Interpretationown data
HFD feeding may partially show a suppression of mitochondrial function.
“These data showed that HFD feeding may partially show a suppression of mitochondrial function.”
Quote in the paperSubstantial claim - Interpretationreasoning
Decreased mitochondrial quality occurred in the skeletal muscles and mitochondria of SOB model zebrafish.
“These findings indicated that a decreased mitochondrial quality occurred in the skeletal muscles and mitochondria of SOB model zebrafish.”
Quote in the paperSubstantial claim - Premisecitation
Impaired mitochondrial function in skeletal muscle is thought to promote muscular atrophy in subjects with obesity.
“Impaired mitochondrial function in skeletal muscle is thought to promote muscular atrophy in subjects with obesity [10].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10] Pileggi, 2021, The lifecycle of skeletal muscle mitochondria in obesity, Obes. Rev. source
Not checked in the free run.
- Premisecitation
The AMPK/SIRT1 pathway maintains cellular energy stores in skeletal muscles.
“The AMPK/SIRT1 pathway maintains cellular energy stores in skeletal muscles [27].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [27] Calbet, 2016, AMPK signaling in skeletal muscle during exercise: Role of reactive oxygen and nitrogen species, Free Radic. Biol. Med. source
Not checked in the free run.
- Premisecitation
The AMPK/SIRT1/PGC1α pathway is inhibited in the skeletal muscles of humans and mice with obesity.
“The AMPK/SIRT1/PGC1α pathway is inhibited in the skeletal muscles of humans and mice with obesity [29,30].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [29] Mortensen, 2009, Genetic and metabolic effects on skeletal muscle AMPK in young and older twins, Am. J. Physiol. Endocrinol. Metab. source
Not checked in the free run.
- cites [30] Shariff, 2020, Celastrol attenuates inflammatory responses in adipose tissues and improves skeletal muscle mitochondrial functions in high fat diet-induced obese rats via upregulation of AMPK/SIRT1 signaling pathways, Eur. J. Pharmacol. source
Not checked in the free run.
- Interpretationreasoning
HFD feeding induced increased protein degradation in zebrafish.
“These findings indicate that increased protein degradation and muscle atrophy were induced by HFD feeding in zebrafish.”
Quote in the paperSubstantial claim - Interpretationreasoning
This reduction in mitochondrial biogenesis may result in decreased ATP synthesis and fatty acid β-oxidation.
“This reduction in mitochondrial biogenesis may result in decreased ATP synthesis and fatty acid β-oxidation.”
Quote in the paperSubstantial claim - Interpretationown data
Skeletal muscle atrophy was associated with mitochondrial dysfunction in HFD-fed SOB model zebrafish.
“These results indicated that skeletal muscle atrophy was associated with mitochondrial dysfunction.”
- Also stated in: § 4. Discussion · plain
“In summary, in HFD-fed SOB model zebrafish, muscle atrophy was related to mitochondrial dysfunction.”
- Also stated in: § 4. Discussion · boosted
“Moreover, we demonstrated that this outcome was related to mitochondrial dysfunction in the muscles of SOB-model zebrafish.”
Quote in the paperSubstantial claim- Rests on an assumption: Whether decreased mitochondrial function is associated with impaired muscle function is unclear.
- Also stated in: § 4. Discussion · plain
- May combine two claims. 9
- Classified as probably not a substantial claim. 7
May combine two claims.
Findingown dataAfter 16 weeks, HFD-fed zebrafish developed characteristics of fatty liver with evident increases in lipid droplets, hepatic steatosis severity, and collagen contents.
“After 16 weeks, HFD-fed zebrafish developed the characteristics of fatty liver with evident increases in lipid droplets, hepatic steatosis severity, and collagen contents (Figure 1E).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataMost mitochondria in the HFD group were degenerated, enlarged, and swollen, and mitochondrial cristae were broken or absent.
“most mitochondria in the HFD group were degenerated, enlarged, and swollen, and the mitochondrial cristae were broken or absent.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
PremisecitationA reduction in muscle mass induced by SOB may contribute to dysregulation of the mitochondrial network and impairment of mitochondrial function.
“The reduction in muscle mass induced by SOB may contribute to dysregulation of the mitochondrial network and impairment of mitochondrial function [10,11].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [10] Pileggi, 2021, The lifecycle of skeletal muscle mitochondria in obesity, Obes. Rev. source
Not checked in the free run.
- cites [11] Huang, 2019, Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway, Aging source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationMany researchers have developed reliable zebrafish models to understand muscle degeneration and its pathophysiology.
“Many researchers have developed reliable zebrafish models to understand muscle degeneration and its pathophysiology [13,14].”
Quote in the paperNot a substantial claim0 of 2 sources checkedClassified as probably not a substantial claim.
PremisecitationMitochondria are crucial organelles responsible for the ATP supply and metabolic status of skeletal muscle.
“Mitochondria are crucial organelles responsible for the ATP supply and metabolic status of skeletal muscle [9].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9] Hood, 2019, Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging, Annu. Rev. Physiol. source
Not checked in the free run.
May combine two claims.
PremisecitationA few weeks of HFD feeding can cause intramyocellular lipid accumulation and reduce mitochondrial function.
“Indeed, a few weeks of HFD feeding can cause intramyocellular lipid accumulation and reduce mitochondrial function [26].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Chen, 2018, Adaptations of Skeletal Muscle Mitochondria to Obesity, Exercise, and Polyunsaturated Fatty Acids, Lipids source
Not checked in the free run.
May combine two claims.
Interpretationown dataLong-term HFD feeding could promote mitochondrial fission and suppress mitochondrial fusion.
“These data suggested that long-term HFD feeding could promote mitochondrial fission and suppress mitochondrial fusion.”
Quote in the paperSubstantial claim- Rests on an assumption: MFN2 is responsible for outer membrane fusion, whereas OPA1 is required for inner membrane fusion.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPGC1α can be stimulated by the AMPK/SIRT1 pathway.
“as the main regulator of mitochondrial biogenesis, PGC1α can be stimulated by the AMPK/SIRT1 pathway [28].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [28] Tang, 2016, Sirt1 and the Mitochondria, Mol. Cells source
Not checked in the free run.
May combine two claims.
PremisecitationLipid overload in skeletal muscle lowers muscle mass and induces sarcopenia.
“Lipid overload in the skeletal muscle lowers muscle mass and induces sarcopenia [19,20].”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationMitochondrial biogenesis is responsible for oxidative phosphorylation and fatty acid β-oxidation.
“mitochondrial biogenesis is responsible for oxidative phosphorylation and fatty acid β-oxidation [31].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [31] Dorn, 2015, Mitochondrial biogenesis and dynamics in the developing and diseased heart, Genes Dev. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationMitochondria are unique and highly dynamic organelles that exhibit continuous fission and fusion.
“Mitochondria are unique and highly dynamic organelles that exhibit continuous fission and fusion [32].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [32] Lee, 2016, Mitochondrial fission and fusion, Biochem. Soc. Trans. source
Not checked in the free run.
Classified as probably not a substantial claim. May combine two claims.
PremisecitationMitochondria play essential roles in regulating fatty acid metabolism and ATP production, which are important for muscle contractibility and plasticity.
“Mitochondria play essential roles in regulating fatty acid metabolism and ATP production, which are important for muscle contractibility and plasticity [25].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Abrigo, 2019, Mitochondrial Dysfunction in Skeletal Muscle Pathologies, Curr. Protein Pept. Sci. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationFusion ameliorates stress by mixing the contents of partially damaged mitochondria as a form of complementation, whereas fission is thought to induce oxidative stress and cell apoptosis.
“Fusion ameliorates stress by mixing the contents of partially damaged mitochondria as a form of complementation, whereas fission is thought to induce oxidative stress and cell apoptosis [33].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [33] Chan, 2020, Mitochondrial Dynamics and Its Involvement in Disease, Annu. Rev. Pathol. source
Not checked in the free run.
The paper relies on this without support.
Whether decreased mitochondrial function is associated with impaired muscle function is unclear.
“however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear.”
The paper relies on this without support.
Zebrafish is a promising model system for studying human diseases such as obesity and sarcopenia because of functional conservation in substance and energy metabolism and similar characteristics in muscular physiology.
“Zebrafish is a promising model system for studying human diseases, such as obesity and sarcopenia, because of the functional conservation in substance and energy metabolism and the similar characteristics in muscular physiology.”
The paper relies on this without support.
MFN2 is responsible for outer membrane fusion, whereas OPA1 is required for inner membrane fusion.
“MFN2 is responsible for outer membrane fusion, whereas OPA1 is required for inner membrane fusion.”
The paper relies on this without support.
Fusion and fission processes regulate the length, size, and morphology of mitochondria, and these mitochondrial dynamics are associated with mitochondrial function.
“Fusion and fission processes regulate the length, size, and morphology of mitochondria, and these mitochondrial dynamics are associated with mitochondrial function.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Lower levels of mitochondrial biogenesis markers AMPK, SIRT1, and PGC1α are detected in the muscles of obese animals.
“In the context of mitochondrial biogenesis regulators, lower levels of mitochondrial biogenesis markers, AMPK, SIRT1, and PGC1α, are detected in the muscles of obese animals [54, 55].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [55]
These lower marker levels are accompanied by significant decreases in expression of genes related to mitochondrial biogenesis, fatty acid oxidation, and ETC complex subunits, indicating an effect of obesity on mitochondrial function.
“These levels are accompanied by significant decreases in the expression of genes related to mitochondrial biogenesis (Nrf, Tfam, Pgc1α, and Sirt1), fatty acid oxidation, and ETC complex subunits, indicating the effect of obesity on mitochondrial function.”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [55]
Obese zebrafish and high-fat diet-fed obese rats exhibit higher expression levels of DRP1 and lower levels of OPA1 and MFN2.
“These obese animals exhibit higher expression levels of DRP1 and lower levels of OPA1 and MFN2 [55, 61].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [55]
Disrupted mitochondrial dynamics results in morphological changes such as degeneration, enlargement, and swelling of mitochondria with disrupted cristae.
“Moreover, the disrupted mitochondrial dynamics results in morphological changes such as degeneration, enlargement, and swelling of mitochondria with disrupted cristae [55].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [55]
The citation lists haven’t been fetched yet
References 34 · Cited by 24
- Authors
- Zou, Y.-Y., Chen, Z.-L., Sun, C.-C., Yang, D., Zhou, Z.-Q., Xiao, Q., Peng, X.-Y., & Tang, C.-F.
- Affiliations
- Hunan Normal University (CN)
- Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2022-05-09
- Volume
- 14
- Issue
- 9
- Pages
- 1975
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC9105418
- OpenAlex
- W4229457177
- Semantic Scholar
- 07e8c71828242271c7aabee7131d1228c0aa2dbb
- Cited by
- 24
- References
- 34
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 5 · 2023: 8 · 2022: 1
- FWCI
- 1.71
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81801392, 32100919, 21B0066, 2019JJ50098, CX20200532, CX20210483)
- Hunan Province Education Department (81801392, 32100919, 21B0066, 2019JJ50098, CX20200532, CX20210483)
- Hunan Provincial Natural Science Foundation of China (81801392, 32100919, 21B0066, 2019JJ50098, CX20200532, CX20210483)
- Postgraduate Scientific Research Innovation Project of Hunan Province (81801392, 32100919, 21B0066, 2019JJ50098, CX20200532, CX20210483)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Keywords
- sarcopenic obesity, high-fat diet, mitochondrial dysfunction, skeletal muscle atrophy, zebrafish model, exercise capacity, mitochondrial biogenesis, fatty acid oxidation, mitochondrial fission and fusion, atrogin-1, muscle fiber cross-sectional area
- MeSH terms
- Animals, Mitochondria, Mitochondria, Muscle, Muscular Atrophy, Obesity, Swimming, Zebrafish, Muscle, Skeletal, Sarcopenia, Diet, High-Fat
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