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Cited by 27Mitochondrial Function and PathologyAdipose Tissue and MetabolismMuscle Physiology and Disorders

Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds

Open access
Jun, Lauren, Tao, Ya-Xiong, Geetha, Thangiah, Babu, Jeganathan Ramesh·2024·Current Nutrition Reports
DOI 10.1007/s13668-024-00555-7PMC PMC11327216
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Abstract

Purpose of Review: The global obesity epidemic has become a major public health concern, necessitating comprehensive research into its adverse effects on various tissues within the human body. Among these tissues, skeletal muscle has gained attention due to its susceptibility to obesity-related alterations. Mitochondria are primary source of energy production in the skeletal muscle. Healthy skeletal muscle maintains constant mitochondrial content through continuous cycle of synthesis and degradation. However, obesity has been shown to disrupt this intricate balance. This review summarizes recent findings on the impact of obesity on skeletal muscle mitochondria structure and function. In addition, we summarize the molecular mechanism of mitochondrial quality control systems and how obesity impacts these systems. Recent Findings: Recent findings show various interventions aimed at mitigating mitochondrial dysfunction in obese model, encompassing strategies including caloric restriction and various dietary compounds. Summary: Obesity has deleterious effect on skeletal muscle mitochondria by disrupting mitochondrial biogenesis and dynamics. Caloric restriction, omega-3 fatty acids, resveratrol, and other dietary compounds enhance mitochondrial function and present promising therapeutic opportunities.

AI snapshot

Written from the paper’s full text.

TL;DR

This narrative review summarizes how obesity disrupts skeletal muscle mitochondrial quality control—biogenesis, fusion/fission, and mitophagy—and discusses caloric restriction and dietary compounds as interventions that may improve mitochondrial function. It concludes that SIRT1/AMPK/PGC1α signaling is a central target, but clinical dosing and precise mechanisms remain unresolved.

Key findings

  • Obesity promotes a skeletal muscle fiber-type shift from oxidative (Type I/IIA) to glycolytic (Type IIB), with lower AMPK, SIRT1, and PGC1α and decreased expression of mitochondrial biogenesis genes (*Nrf*, *Tfam*, *Pgc1α*, *Sirt1*), fatty acid oxidation genes, and ETC subunits.
  • Obesity alters mitochondrial dynamics: human morbid obesity shows elevated fasting plasma free fatty acids correlated with mitochondrial fragmentation, downregulated MFN1/MFN2, and upregulated DRP1; obese zebrafish and high-fat-fed rats show higher DRP1 and lower OPA1/MFN2.
  • Caloric restriction and dietary compounds show promise: e.g., 20 days of 60% ad libitum intake increased skeletal muscle SIRT1 deacetylase activity; 6 months of 25% caloric reduction improved mitochondrial biogenesis markers; 150 mg/day resveratrol for 30 days reduced blood glucose and insulin in healthy obese men; 100 mg/kg/day resveratrol for 8 weeks protected against high-fat diet-induced intramuscular lipid accumulation and insulin resistance; omega-3 and berberine/quercetin also improved mitochondrial markers in animal or cell studies.
  • The review identifies SIRT1/AMPK/PGC1α as a shared pathway through which caloric restriction, resveratrol, omega-3 fatty acids, berberine, and flavonoids may enhance mitochondrial biogenesis and reduce ROS/inflammatory cytokines.

Methods

  • Design: narrative review of recent findings on obesity, skeletal muscle mitochondria, mitochondrial quality control, and dietary interventions.
  • Data/sample: no primary data; synthesizes animal, cell, and human studies, including obese models, high-fat diet models, caloric restriction studies, and nutraceutical trials.
  • Analysis: descriptive synthesis organized around mitochondrial biogenesis, mitophagy, fusion/fission, obesity effects, and therapeutic approaches; includes schematic figures for mitochondrial dynamics/mitophagy, biogenesis, and dietary compound effects.

Limitations

  • Stated: the precise molecular associations between lifestyle modifications, nutraceuticals, and obesity-induced mitochondrial dysfunction remain elusive; future studies are needed.
  • Stated: the optimal dose of resveratrol remains elusive in clinical practice, and some studies report insufficient effects; human trials should consider bioavailability and pharmacokinetics.
  • Stated: caloric restriction effects on mitochondrial content and function remain controversial, with discrepancies attributed to study duration, interpretation of transcriptional markers, and subcellular localization of PGC1α.
  • Evident: as a narrative review, it does not report a systematic search strategy, risk-of-bias assessment, or meta-analysis, and many findings rely on animal or cell models with limited human clinical data.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1007/s13668-024-00555-7

Cites

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Statistics

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Claims the paper makes

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  • Premisecitation

    Impaired mitochondrial function directs fatty acids toward storage rather than oxidation, contributing considerably to intramyocellular lipid accumulation and insulin resistance.

    “Indeed, impaired mitochondrial function directs fatty acids toward storage, as opposed to oxidation, which contributes considerably to intramyocellular lipid accumulation and insulin resistance [16].”
    Quote in the paperSubstantial claim0 of 1 sources checked
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  • Premisecitation

    Skeletal muscle experiences elevated ROS production due to cellular responses to elevated free fatty acids and hyperglycemia in obesity.

    “Notably, skeletal muscle experiences an elevated ROS production due to cellular responses to elevated levels of free fatty acids and hyperglycemia in obesity [18, 19].”
    Quote in the paperSubstantial claim0 of 2 sources checked
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  • Premisecitation

    Obesity and insulin resistance contribute to muscle fiber type switch from oxidative to glycolytic type.

    “Thus, it is not surprising that obesity and insulin resistance contribute to muscle fiber type switch from oxidative to glycolytic type [9].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
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  • Premisecitation

    There is evidence suggesting a disruption in mitophagy in aged skeletal muscle.

    “While previous reports remain conflicting, there are evidence suggesting a disruption in mitophagy in the skeletal muscle in obesity [26], long-term high-fat diet consumption [27], and aged skeletal muscle [22, 23].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
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  • Premisecitation

    Dysregulated mitophagy can impact mitochondrial quantity and function.

    “Dysregulated mitophagy, however, can impact the mitochondrial quantity and function [19].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [19] de Mello AH, Costa AB, Engel JDG, Rezin GT. Mitochondrial dysfunction in obesity. Life Sci. 2018;192:26–32. https://doi.org/10.1016/j.lfs.2017.11.019. source

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  • Classified as probably not a substantial claim. 7

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    Premisecitation

    Prolonged high-fat diet exposure gradually decreases the early oxidative adaptation, ultimately resulting in fiber type shift toward glycolytic fibers and eventual development of insulin resistance.

    “This adaptation, however, gradually decreases with prolonged high-fat diet exposure, ultimately resulting in fiber type shift towards glycolytic fibers and the eventual development of insulin resistance [8, 9].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [8] Moreno M, et al. 3,5-Diiodo-L-thyronine prevents high-fat-diet-induced insulin resistance in rat skeletal muscle through metabolic and structural adaptations. FASEB J. 2011;25:3312–24. https://doi.org/10.1096/fj.11-181982. source

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    • cites [9] Umek N, Horvat S, Cvetko E. Skeletal muscle and fiber type-specific intramyocellular lipid accumulation in obese mice. Bosn J Basic Med Sci. 2021. https://doi.org/10.17305/bjbms.2021.5876. This article demonstrates intramyocellular lipid accumulation specific to muscle- and fiber-type in obese mouse model. source

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    Premisecitation

    Mitochondrial dysfunction in obesity leads to decreased mitochondrial content, decreased genetic material, and decreased rate of OXPHOS.

    “Ultimately, this dysfunction leads to decreased mitochondrial content, decreased genetic material, and decreased rate of OXPHOS [19, 20].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [19] de Mello AH, Costa AB, Engel JDG, Rezin GT. Mitochondrial dysfunction in obesity. Life Sci. 2018;192:26–32. https://doi.org/10.1016/j.lfs.2017.11.019. source

      Not checked in the free run.

    • cites [20] Heinonen S, et al. Impaired mitochondrial biogenesis in adipose tissue in acquired obesity. Diabetes. 2015;64:3135–45. https://doi.org/10.2337/db14-1937. source

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  • Probably not a substantial claim: may not pass S4 (based).

    Premisenone given

    Obesity exerts deleterious consequences on specific tissues, including skeletal muscle.

    “Beyond these systemic effects, obesity also exerts deleterious consequences on specific tissues, including the skeletal muscle.”
    Quote in the paperNot a substantial claim

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    Premisecitation

    The AMPKα1 catalytic subunit potentiates myogenic expression, myogenesis, and muscle regeneration.

    “This AMPK-mediated muscle cell regeneration is supported by the fact that AMPKα1 catalytic subunit potentiates myogenic expression, myogenesis, and muscle regeneration [59].”
    Quote in the paperSubstantial claim0 of 1 sources checked
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    Premisecitation

    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.”
    Quote in the paperSubstantial claim0 of 2 sources checked
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    Interpretationcitation

    AMPK regulates mitochondrial oxidative capacity and substrate utilization without influencing baseline mitochondrial content.

    “highlighting AMPK’s role in regulating mitochondrial oxidative capacity and substrate utilization without influencing the baseline mitochondrial content.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [35] Lantier L, et al. AMPK controls exercise endurance, mitochondrial oxidative capacity, and skeletal muscle integrity. FASEB J. 2014;28:3211–24. https://doi.org/10.1096/fj.14-250449. source

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    Premisecitation

    Activation of AMPK increased the density of quiescent satellite cells, enhanced satellite cell proliferation, and promoted satellite cell myogenic differentiation in regenerating muscle.

    “This was confirmed when activation of AMPK increased the density of quiescent satellite cells, enhanced satellite cell proliferation, and promoted satellite cell myogenic differentiation in regenerating muscle [57].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [57] Niu W, Wang H, Wang B, Mao X, Du M. Resveratrol improves muscle regeneration in obese mice through enhancing mitochondrial biogenesis. J Nutr Biochem. 2021;98. https://doi.org/10.1016/j.jnutbio.2021.108804.This article explores the ability of resveratrol to enhance muscle regeneration affected by obesity, focusing on the mitochondrial biogenesis signaling pathway that involves AMPK/PGC-1. source

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    Premisecitation

    Obesity inhibits AMPK activity, negatively impacting PGC1α transcription and co-activator functions, thereby impairing mitochondrial biogenesis in skeletal muscle.

    “Obesity inhibits AMPK activity, which negatively impacts PGC1α transcription and its co-activator functions, [57] thereby impairing mitochondrial biogenesis in skeletal muscle.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [57] Niu W, Wang H, Wang B, Mao X, Du M. Resveratrol improves muscle regeneration in obese mice through enhancing mitochondrial biogenesis. J Nutr Biochem. 2021;98. https://doi.org/10.1016/j.jnutbio.2021.108804.This article explores the ability of resveratrol to enhance muscle regeneration affected by obesity, focusing on the mitochondrial biogenesis signaling pathway that involves AMPK/PGC-1. source

      Not checked in the free run.

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    Premisecitation

    Mitochondrial fission is a quality control mechanism that isolates damaged or dysfunctional mitochondrial segments for removal by mitophagy.

    “Furthermore, mitochondrial fission is another important quality control mechanism, isolating damaged or dysfunctional mitochondrial segments for removal by mitophagy [45].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [45] Chen H, Vermulst M, Wang YE, Chomyn A, Prolla TA, McCaffery JM, Chan DC. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell. 2010;141:280–9. https://doi.org/10.1016/j.cell.2010.02.026. source

      Not checked in the free run.

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    Premisecitation

    Skeletal muscle exhibits a high abundance of MFN2, and disruption of MFN2 is related to disruption in mitochondrial membrane potential and cellular oxygen consumption.

    “Skeletal muscle exhibits a high abundance of MFN2, and disruption of this protein have been related to disruption in mitochondrial membrane potential and cellular oxygen consumption [46].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [46] Zorzano A, Liesa M, Palacín M. Role of mitochondrial dynamics proteins in the pathophysiology of obesity and type 2 diabetes. Int J Biochem Cell Biol. 2009;41:1846–54. https://doi.org/10.1016/j.biocel.2009.02.004. source

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    Premisecitation

    Disruptions in mitochondrial dynamics can lead to aberrant mitochondrial morphology, compromised respiratory function, and decreased ATP content in skeletal muscle.

    “Disruptions in mitochondrial dynamics can lead to aberrant mitochondrial morphology, compromised respiratory function, and decreased ATP content in skeletal muscle [60].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [60] Liu R, et al. Impaired mitochondrial dynamics and bioenergetics in diabetic skeletal muscle. PLoS ONE. 2014;9:e92810. https://doi.org/10.1371/journal.pone.0092810. source

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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    DRP1 is recruited to marked division sites, binds OMM receptors and adaptors Mff and Fis1, and this binding facilitates DRP1 oligomerization into a ring-like structure that promotes complete mitochondrial division.

    “Subsequently, DRP1 is recruited to these marked division sites, binding to its OMM receptors and adaptors, namely mitochondrial fission factor (Mff) and fission protein 1 (Fis1). This binding event facilitates the oligomerization of DRP1, leading to the formation of a ring-like structure that promotes complete division of the mitochondria [15].”
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      Not checked in the free run.

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    Premisecitation

    Mitochondrial fusion prior to reaching the critical threshold stabilizes mtDNA copy number and prevents accumulation of mtDNA mutations.

    “This protective mechanism of mitochondrial fusion, prior to reaching the critical threshold, primarily operates through stabilizing mtDNA copy number and preventing the accumulation of mtDNA mutations [45].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [45] Chen H, Vermulst M, Wang YE, Chomyn A, Prolla TA, McCaffery JM, Chan DC. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell. 2010;141:280–9. https://doi.org/10.1016/j.cell.2010.02.026. source

      Not checked in the free run.

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    Premisecitation

    Mitochondrial fission initiates with mitochondria establishing contact with the endoplasmic reticulum (ER), which is crucial for identifying the scission site within the mitochondrial network.

    “The fission initiates with mitochondria establishing contact with the endoplasmic reticulum (ER), a crucial player in identifying the scission site within the mitochondrial network [48].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [48] Friedman JR, Lackner LL, West M, DiBenedetto JR, Nunnari J, Voeltz GK. ER tubules mark sites of mitochondrial division. Science. 2011;1979(334):358–62. https://doi.org/10.1126/science.1207385. source

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    Premisecitation

    Overexpression of PGC1α promotes glycolytic-to-oxidative fiber-type shift and mitochondrial biogenesis in skeletal muscle.

    “In this regard, overexpression of PGC1α promotes glycolytic-to-oxidative fiber-type shift and mitochondrial biogenesis in skeletal muscle [58].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [58] Lin J, Puigserver P, Donovan J, Tarr P, Spiegelman BM. Peroxisome proliferator-activated receptor γ coactivator 1β (PGC-1β), a novel PGC-1-related transcription coactivator associated with host cell factor. J Bio Chem. 2002;277:1645–8. https://doi.org/10.1074/jbc.C100631200. source

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    Interpretationnone given

    Obesity induces fission of mitochondria into smaller fragmented organelles, resulting in diminished insulin sensitivity and OXPHOS, ultimately leading to muscle fiber type switch toward glycolytic fibers.

    “Obesity induces the fission of mitochondria into smaller fragmented organelles, resulting in diminished insulin sensitivity and OXPHOS, ultimately leading to muscle fiber type switch towards glycolytic fibers.”
    Quote in the paperNot a substantial claim

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    Premisecitation

    Mice with skeletal muscle-specific deletion of Mfn2 exhibit impaired mitochondrial morphology, localization, and calcium uptake, ultimately resulting in decreased muscle cross-sectional area and strength.

    “Mice with skeletal muscle-specific deletion of Mfn2 exhibit impaired mitochondrial morphology, localization, and calcium uptake, ultimately resulting in decreased muscle cross-sectional area and strength.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [46] Zorzano A, Liesa M, Palacín M. Role of mitochondrial dynamics proteins in the pathophysiology of obesity and type 2 diabetes. Int J Biochem Cell Biol. 2009;41:1846–54. https://doi.org/10.1016/j.biocel.2009.02.004. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based). May combine two claims.

    Interpretationnone given

    Obesity inhibits mitophagy, leading to accumulation of dysfunctional mitochondria.

    “Obesity inhibits mitophagy, leading to accumulation of dysfunctional mitochondria.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    SIRT1 transgenic muscle exhibits a shift from fast-to-slow twitch fiber types, increased PGC1α levels, and decreased expression of muscle atrophy markers.

    “Notably, SIRT1 transgenic muscle exhibits a shift from fast-to-slow twitch fiber types, increased PGC1α levels, and decreased expression of muscle atrophy markers [41].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [41] Chalkiadaki A, Igarashi M, Nasamu AS, Knezevic J, Guarente L. Muscle-specific SIRT1 gain-of-function increases slow-twitch fibers and ameliorates pathophysiology in a mouse model of Duchenne muscular dystrophy. PLoS Genet. 2014;10:e1004490. https://doi.org/10.1371/journal.pgen.1004490. source

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    Interpretationreasoning

    Alteration in fiber type proportion impacts whole body metabolism and accelerates the development of insulin resistance.

    “Therefore, the alteration in fiber type proportion impacts whole body metabolism and accelerates the development of insulin resistance.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Skeletal muscle-specific AMPKα1α2 double-knockout mice show diminished maximal ADP-stimulated mitochondrial respiration without alterations in mitochondrial numbers.

    “Intriguingly, these mice show diminished maximal ADP-stimulated mitochondrial respiration without alterations in mitochondrial numbers, highlighting AMPK’s role in regulating mitochondrial oxidative capacity and substrate utilization without influencing the baseline mitochondrial content.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [35] Lantier L, et al. AMPK controls exercise endurance, mitochondrial oxidative capacity, and skeletal muscle integrity. FASEB J. 2014;28:3211–24. https://doi.org/10.1096/fj.14-250449. source

      Not checked in the free run.

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    Premisecitation

    High-fat diet-induced obese mice exhibited decreased mtDNA content, expression of PGC1α, and several mitochondrial markers.

    “High-fat diet-induced obese mice exhibited decreased mtDNA content, expression of PGC1α, and several mitochondrial markers.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [57] Niu W, Wang H, Wang B, Mao X, Du M. Resveratrol improves muscle regeneration in obese mice through enhancing mitochondrial biogenesis. J Nutr Biochem. 2021;98. https://doi.org/10.1016/j.jnutbio.2021.108804.This article explores the ability of resveratrol to enhance muscle regeneration affected by obesity, focusing on the mitochondrial biogenesis signaling pathway that involves AMPK/PGC-1. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Upon reintroduction of MFN2, oxidative stress and insulin resistance are alleviated.

    “Upon reintroduction of MFN2, the oxidative stress and insulin resistance are alleviated [47].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [47] Nie Q, et al. Mitofusin 2 deficiency leads to oxidative stress that contributes to insulin resistance in rat skeletal muscle cells. Mol Biol Rep. 2014;41:6975–83. https://doi.org/10.1007/s11033-014-3584-9. source

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    Premisecitation

    Conditional deletion of Mfn1 and Mfn2 results in severe mtDNA depletion in muscle and causes severe mitochondrial dysfunction, compensatory mitochondrial proliferation, and muscle atrophy.

    “Indeed, conditional deletion of Mfn1 and Mfn2 results in severe mtDNA depletion in muscle and causes severe mitochondrial dysfunction, compensatory mitochondrial proliferation, and muscle atrophy [45].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [45] Chen H, Vermulst M, Wang YE, Chomyn A, Prolla TA, McCaffery JM, Chan DC. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell. 2010;141:280–9. https://doi.org/10.1016/j.cell.2010.02.026. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    An obesity-resistant lean phenotype tends to have higher expression of mitochondrial biogenesis markers, indicating a potential relationship between skeletal muscle mitochondrial biogenesis and the onset of obesity and obesity-resistance during high-fat diet feeding.

    “Notably, obesity-resistant lean phenotype tends to have a higher expression of mitochondrial biogenesis markers, indicating potential relationship between mitochondrial biogenesis in skeletal muscle and the onset of obesity and obesity-resistance development in the course of high-fat diet feeding [56].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [56] Sun J, et al. Early mitochondrial adaptations in skeletal muscle to obesity and obesity resistance differentially regulated by high-fat diet. Exp Clin Endocrinol. 2017;125:538–46. https://doi.org/10.1055/s-0043-104634. source

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    Premisecitation

    Knockout models with mtDNA depletion show a progressive decline in exercise performance, accompanied by impaired electron transport chain, particularly for complex I and IV.

    “As result of mtDNA depletion, studies with knockout models also show a progressive decline in exercise performance, accompanied by impaired electron transport chain, particularly for complex I and IV [43].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [43] Chen W, Zhao H, Li Y. Mitochondrial dynamics in health and disease: Mechanisms and potential targets. Sig Transduct Target Ther. 2023;8:333. https://doi.org/10.1038/s41392-023-01547-9. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

    Interpretationnone given

    Elongated mitochondria are predominant in type I and IIA muscle fibers, contributing to increased insulin sensitivity and OXPHOS.

    “Elongated mitochondria are predominant in type I and IIA muscle fibers, contributing to increased insulin sensitivity and OXPHOS.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Lipotoxicity associated with obesity inhibits autophagic flux, and defective degradation is the main cause of autophagosome accumulation in tissues of obese models.

    “Indeed, later studies showed that lipotoxicity associated with obesity inhibits the autophagic flux and defective degradation is the main cause of autophagosome accumulation in the tissues of obese model [28].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [28] Namkoong S, Cho CS, Semple I, Lee JH. Autophagy Dysregulation and Obesity-Associated Pathologies. Mol Cells. 2018;41:3–10. https://doi.org/10.14348/molcells.2018.2213. source

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    Premisecitation

    The shift toward type II fiber growth is a protective mechanism to sustain metabolic homeostasis, mediated by Baf60c.

    “This shift, particularly the growth of type II fiber, is a protective mechanism to sustain metabolic homeostasis, which is mediated by Brg1/Brm-associated factor (Baf60c) [51].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [51] Sinha I, Sakthivel D, Varon DE. Systemic regulators of skeletal muscle regeneration in obesity. Front Endocrinol (Lausanne). 2017;8. https://doi.org/10.3389/fendo.2017.00029. source

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    Premisecitation

    Co-transfecting mitochondria with DRP1 and FIS1 induces alterations in mitochondrial morphology and activates autophagy.

    “Romanello et al. reported that co-transfecting mitochondria with DRP1 and FIS1 induces alterations in mitochondrial morphology and activates autophagy [50].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [50] Romanello V, et al. Mitochondrial fission and remodeling contributes to muscle atrophy. EMBO J. 2010;29:1774–85. https://doi.org/10.1038/emboj.2010.60. source

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    Premisecitation

    In L6 cells treated with palmitate and siMfn2, repression of Mfn2 mRNA expression coincides with reduced mitochondrial membrane potential and antioxidant enzyme activities, resulting in elevated ROS production and phosphorylation of inflammatory cytokines.

    “In L6 cells treated with palmitate and small interfering RNA (siMfn2), repression of Mfn2 mRNA expression coincides with reduced mitochondrial membrane potential and antioxidant enzyme activities, resulting in elevated ROS production and the phosphorylation of inflammatory cytokines.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [47] Nie Q, et al. Mitofusin 2 deficiency leads to oxidative stress that contributes to insulin resistance in rat skeletal muscle cells. Mol Biol Rep. 2014;41:6975–83. https://doi.org/10.1007/s11033-014-3584-9. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Deacetylase activity of SIRT1 in skeletal muscle is increased in animals on a 20-day caloric restriction diet (60% of ad libitum intake), concomitant with enhanced insulin signaling and glucose uptake.

    “Notably, deacetylase activity of SIRT1 in skeletal muscle is increased in animals on a 20-day caloric restriction diet (60% of ad libitum intake), concomitant with enhanced insulin signaling and glucose uptake [72].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [72] Schenk S, et al. Sirt1 enhances skeletal muscle insulin sensitivity in mice during caloric restriction. JCI. 2011;121:4281–8. https://doi.org/10.1172/JCI58554. source

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    Premisecitation

    In an animal study, 100 mg/kg of daily resveratrol treatment for eight weeks protected against high-fat diet-induced intramuscular lipid accumulation and insulin resistance and reverted the decline in SS mitochondrial β-oxidation.

    “In an animal study, 100 mg/kg of daily resveratrol treatment for eight weeks protected against high-fat diet-induced intramuscular lipid accumulation and insulin resistance and reverts the decline in SS mitochondrial β-oxidation [87].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [87] Chen L-L, et al. Resveratrol attenuates high-fat diet–induced insulin resistance by influencing skeletal muscle lipid transport and subsarcolemmal mitochondrial β-oxidation. Metabolism. 2011;60:1598–609. https://doi.org/10.1016/j.metabol.2011.04.002. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a study by Sparks et al., only subjects with baseline "more coupled" mitochondria benefited from caloric restriction, with improvements in muscle mitochondrial ATP synthesis rates and coupling.

    “In a study by Sparks et al., only those subjects with a baseline of “more coupled” mitochondria benefited from caloric restriction, with improvements in muscle mitochondrial ATP synthesis rates and coupling [77].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [77] Liu B, Hutchison AT, Thompson CH, Lange K, Wittert GA, Heilbronn LK. Effects of intermittent fasting or calorie restriction on markers of lipid metabolism in human skeletal muscle. J Clin Endocrinol Metab. 106:E1389-E1399. https://doi.org/10.1210/clinem/dgaa707. source

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  • May combine two claims.

    Premisecitation

    Caloric restriction and natural compounds elicit changes in cellular mitochondrial content and mitigate mitochondrial ROS production.

    “A common theme emerging from studies is that caloric restriction and these natural compounds elicit changes in cellular mitochondrial content and mitigates mitochondrial ROS production [69].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [69] Vásquez-Reyes S, Velázquez-Villegas LA, Vargas-Castillo A, Noriega LG, Torres N, Tovar AR. Dietary bioactive compounds as modulators of mitochondrial function. J Nutr Biochem. 2021;96. https://doi.org/10.1016/j.jnutbio.2021.108768. This review article summarizes evidence supporting the impact of dietary bioactive compounds on mitochondrial function. Moreover, it discusses the relationship between these effects and various pathological states. source

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  • May combine two claims.

    Premisecitation

    Thirty-six weeks of 60% caloric restriction enhances transcription levels of genes involved in ROS scavenger function and energy metabolism without altering mitochondrial function and enzyme activities.

    “Similarly, a separate study reports that a 36 weeks of 60% caloric restriction enhances the transcription levels of genes involved in ROS scavenger function and energy metabolism without altering mitochondrial function and enzyme activities [75].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [75] Sreekumar R, et al. Effects of caloric restriction on mitochondrial function and gene transcripts in rat muscle. Am J Physiol Endocrinol Metab. 2002;283:E38–43. https://doi.org/10.1152/ajpendo.00387.2001. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In animal studies, resveratrol treatment increases mitochondrial content and prevents alterations in mitochondrial morphology in muscles caused by high-fat diet and diabetic condition.

    “In animal studies, resveratrol treatment increases mitochondrial content and prevents alterations in mitochondrial morphology in the muscles caused by high-fat diet (in 0.4% concentration for ten weeks) [61] and diabetic condition (in 0.04% concentration for eight weeks) [86].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [61] Huang Y, et al. Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway. Aging. 2019;11:2217–40. https://doi.org/10.18632/aging.101910. source

      Not checked in the free run.

    • cites [86] Wang D, et al. Resveratrol improves muscle atrophy by modulating mitochondrial quality control in STZ‐induced diabetic mice. Mol Nutr Food Res. 2018;62. https://doi.org/10.1002/mnfr.201700941. source

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  • May combine two claims.

    Premisecitation

    Caloric restriction is effective in ameliorating obesity-related metabolic impairments and increasing mitochondrial biogenesis markers, primarily through metabolic pathways involving AMPK and SIRT1.

    “Nonetheless, caloric restriction is effective in ameliorating obesity-related metabolic impairments and increasing mitochondrial biogenesis markers, primarily through metabolic pathways involving AMPK and SIRT1 [80].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [80] Kitada M, Kume S, Takeda-Watanabe A, Tsuda S, Kanasaki K, Koya D. Calorie restriction in overweight males ameliorates obesity-related metabolic alterations and cellular adaptations through anti-aging effects, possibly including AMPK and SIRT1 activation. Biochim Biophys Acta. 2013;1830:4820–7. https://doi.org/10.1016/j.bbagen.2013.06.014. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Thirty percent caloric restriction mice show increased levels of PGC1α, several mitochondrial associated proteins, and cytochrome c oxidase content in skeletal muscle.

    “Hempenstall et al. corroborated these findings, observing increased levels of PGC1α, several mitochondrial associated proteins, and cytochrome c oxidase content in skeletal muscle of 30% caloric restriction mice [76].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [76] Hempenstall S, Page MM, Wallen KR, Selman C. Dietary restriction increases skeletal muscle mitochondrial respiration but not mitochondrial content in C57BL/6 mice. Mech Ageing Dev. 2012;133:37–45. https://doi.org/10.1016/j.mad.2011.12.002. source

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  • May combine two claims.

    Premisecitation

    Caloric restriction remodeling makes mitochondria more efficient, with an increased proportion of respiration coupled to ATP production and reduced overall oxygen consumption and ROS production.

    “This remodeling makes mitochondria more efficient – increased proportion of respiration coupled to ATP production and reduced overall oxygen consumption and producing less ROS [71]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [71] Sparks LM, et al. Effects of 12 months of caloric restriction on muscle mitochondrial function in healthy individuals. J Clin Endocrinol Metab. 2016;102:111–21. https://doi.org/10.1210/jc.2016-3211. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    MFN2-knockout mice exhibited enhanced hepatic glucose production and impaired response to insulin.

    “For instance, MFN2-knockout mice exhibited enhanced hepatic glucose production and impaired response to insulin [67, 68].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [67] Sebastián D, et al. Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis. PNAS. 2012;109:5523–8. https://doi.org/10.1073/pnas.1108220109. source

      Not checked in the free run.

    • cites [68] Kong D, et al. Overexpression of mitofusin 2 improves translocation of glucose transporter 4 in skeletal muscle of high-fat diet-fed rats through AMP-activated protein kinase signaling. Mol Med Rep. 2013;8:205–10. https://doi.org/10.3892/mmr.2013.1457. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In yeast, resveratrol extends lifespan, implicating potential as an anti-aging agent.

    “In yeast, resveratrol has demonstrated its capacity to extend lifespan, implicating the potential of resveratrol as an anti-aging agent [81] with potential clinical implications.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [81] Borra MT, Smith BC, Denu JM. Mechanism of human SIRT1 activation by resveratrol. J Biol Chem. 2005;280:17187–95. https://doi.org/10.1074/jbc.M501250200. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Middle-aged rats on 14 weeks of 40% caloric restriction displayed lower glucose metabolism enzymes than the ad libitum group, implicating metabolic pathway reprogramming from glycolysis to OXPHOS.

    “In another study, middle-aged rats on 14 weeks of 40% caloric restriction displayed lower glucose metabolism enzymes than the ad libitum group [73], implicating metabolic pathway reprogramming from glycolysis to OXPHOS.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [73] Chen C-N, Lin S-Y, Liao Y-H, Li Z-J, Wong AM-K. Late-onset caloric restriction alters skeletal muscle metabolism by modulating pyruvate metabolism. Am J Physiol Endocrinol Metab. 2015;308:E942–9. https://doi.org/10.1152/ajpendo.00508.2014. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Varying results on mitochondrial dynamics proteins may be attributed to differences in diet duration and body weight changes, suggesting that fusion and fission processes occur at distinct time intervals.

    “These varying results may be attributed to differences in diet duration and body weight changes [66], suggesting that fusion and fission processes occur at distinct time intervals.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [66] Jheng H-F, et al. Mitochondrial fission contributes to mitochondrial dysfunction and insulin resistance in skeletal muscle. Mol Cell Biol. 2012;32:309–19. https://doi.org/10.1128/MCB.05603-11. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Resveratrol activates SIRT1, enhancing SIRT1-dependent cellular processes such as axonal protection, fat mobilization, and inhibition of NFκB-dependent transcription.

    “A key property of resveratrol is the activation of SIRT1, enhancing SIRT1-dependent cellular processes such as axonal protection, fat mobilization, and inhibition of NFκB-dependent transcription [81].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [81] Borra MT, Smith BC, Denu JM. Mechanism of human SIRT1 activation by resveratrol. J Biol Chem. 2005;280:17187–95. https://doi.org/10.1074/jbc.M501250200. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Dietary resveratrol supplementation has anti-obesity effects, potentially by mimicking metabolic effects of long-term caloric restriction and improving adipose tissue function and insulin sensitivity in obese models.

    “Recent studies have also revealed anti-obesity effects of dietary resveratrol supplementation [82, 83], potentially by mimicking the metabolic effects of long-term caloric restriction [84] and improving adipose tissue function and insulin sensitivity in obese model [85].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [82] Wang P, Li D, Ke W, Liang D, Hu X, Chen F. Resveratrol-induced gut microbiota reduces obesity in high-fat diet-fed mice. Int J Obes. 2020;44:213–25. https://doi.org/10.1038/s41366-019-0332-1. source

      Not checked in the free run.

    • cites [83] Aguirre L, Fernández-Quintela A, Arias N, Portillo M. Resveratrol: Anti-obesity mechanisms of action. Molecules. 2014;19:18632–55. https://doi.org/10.3390/molecules191118632. source

      Not checked in the free run.

    • cites [84] Timmers S, et al. Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab. 2011;14:612–22. https://doi.org/10.1016/j.cmet.2011.10.002. source

      Not checked in the free run.

    • cites [85] Scapagnini G, et al. Dose response biology of resveratrol in obesity. J Cell Commun Signal. 2014;8:385–91. https://doi.org/10.1007/s12079-014-0257-3. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    SS mitochondria are the main energy provider related to substrate oxidation and insulin action, while IMF mitochondria play a more direct role in supporting muscle contractions.

    “This is not surprising because SS mitochondria are the main energy provider related to substrate oxidation and insulin action, while IMF mitochondria play a more direct role in supporting muscle contractions [88].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [88] Haohao Z, Guijun Q, Juan Z, Wen K, Lulu C. Resveratrol improves high-fat diet induced insulin resistance by rebalancing subsarcolemmal mitochondrial oxidation and antioxidation. J Physiol Biochem. 2015;71:121–31. https://doi.org/10.1007/s13105-015-0392-1. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Moderate reduction of calorie intake to 30-50% less than ad libitum without malnutrition can delay the onset of age-related diseases, improve stress resistance, and slow functional decline.

    “Moderate reduction of calorie intake to 30–50% less than ad libitum without malnutrition can delay the onset of age-related diseases, improve stress resistance, and slow functional decline [70].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [70] Lanza IR, et al. Chronic caloric restriction preserves mitochondrial function in senescence without increasing mitochondrial biogenesis. Cell Metab. 2012;16:777–88. https://doi.org/10.1016/j.cmet.2012.11.003. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    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].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [55] Zou Y-Y, et al. A high-fat diet induces muscle mitochondrial dysfunction and impairs swimming capacity in zebrafish: A new model of sarcopenic obesity. Nutrients. 2022;14:1975. https://doi.org/10.3390/nu14091975. source

      Not checked in the free run.

    • cites [61] Huang Y, et al. Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway. Aging. 2019;11:2217–40. https://doi.org/10.18632/aging.101910. source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Interpretationnone given

    The precise molecular associations between lifestyle modifications, nutraceuticals, and obesity-induced mitochondrial dysfunction remain elusive.

    “While these interventions show promise in in vivo and ex vivo studies, the precise molecular associations between lifestyle modifications, nutraceuticals, and obesity-induced mitochondrial dysfunction remain elusive.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Resveratrol up-regulates expression of genes associated with mitochondrial oxidative phosphorylation while down-regulating those involved in inflammation.

    “Additionally, resveratrol up-regulates the expression of genes associated with mitochondrial oxidative phosphorylation, while down-regulating those involved in inflammation [84].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [84] Timmers S, et al. Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab. 2011;14:612–22. https://doi.org/10.1016/j.cmet.2011.10.002. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Activation of AMPK by berberine may be dependent on SIRT1, as SIRT1-knockdown cells blocked AMPK activation and prevented the effect of berberine on diet-induced insulin resistance.

    “Notably, the activation of AMPK by berberine may be dependent on SIRT1, as SIRT1-knockdown cells blocked AMPK activation and prevented the effect of berberine on diet-induced insulin resistance [95].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [95] Gomes AP, et al. Berberine protects against high fat diet-induced dysfunction in muscle mitochondria by inducing SIRT1-dependent mitochondrial biogenesis. Biochim Biophys Acta. 2012;1822:185–95. https://doi.org/10.1016/j.bbadis.2011.10.008. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Resveratrol treatment may rebalance oxidative stress and antioxidant competence, preserve mitochondrial morphology by stimulating mitochondrial bioenergetics and biogenesis, reverse SS mitochondrial damage, and enhance insulin signaling, eventually improving systemic and skeletal muscle insulin resistance.

    “In summary, resveratrol treatment may rebalance oxidative stress and antioxidant competence, preserve mitochondrial morphology by stimulating mitochondrial bioenergetics and biogenesis, reverse the SS mitochondrial damage, and enhance insulin signaling, eventually improving systemic and skeletal muscle insulin resistance.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Omega-3 PUFAs downregulated mitochondrial fission proteins and improved insulin signaling, suggesting that the anti-obesity effects of omega-3 on insulin resistance development may be partly due to changes in mitochondrial dynamic behavior in skeletal muscle.

    “Additionally, omega-3 PUFAs also downregulated mitochondrial fission proteins and improved insulin signaling, suggesting that the anti-obesity effects of omega-3 on insulin resistance development may be partly due to changes in mitochondrial dynamic behavior in skeletal muscle [93].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [93] Lionetti L, Sica R, Mollica MP, Putti R. High-lard and high-fish-oil diets differ in their effects on insulin resistance development, mitochondrial morphology and dynamic behaviour in rat skeletal muscle. Food Nutr Sci. 2013;4:105–12. https://doi.org/10.4236/fns.2013.49A1017. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Berberine supplementation protects from high-fat diet-induced mitochondrial dysfunction and hyperglycemia in skeletal muscle, partially attributed to an increase in mitochondrial biogenesis.

    “While the precise mechanisms of berberine needs further exploration, recent reports show that berberine supplementation protects from high-fat diet-induced mitochondrial dysfunction and hyperglycemia in skeletal muscle, partially attributed to an increase in mitochondrial biogenesis [95].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [95] Gomes AP, et al. Berberine protects against high fat diet-induced dysfunction in muscle mitochondria by inducing SIRT1-dependent mitochondrial biogenesis. Biochim Biophys Acta. 2012;1822:185–95. https://doi.org/10.1016/j.bbadis.2011.10.008. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In muscle biopsy of healthy obese males supplemented with resveratrol, increased AMPK phosphorylation, SIRT1 and PGC1α expression, and citrate synthase activity were reported.

    “In the muscle biopsy of healthy obese males supplemented with resveratrol, increased AMPK phosphorylation, SIRT1 and PGC1α expression, and citrate synthase activity were reported [84].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [84] Timmers S, et al. Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab. 2011;14:612–22. https://doi.org/10.1016/j.cmet.2011.10.002. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Omega-3 fatty acid treatment enhances mitochondrial biogenesis and oxidative metabolism.

    “In several studies, omega-3 fatty acid treatment has been shown to enhance mitochondrial biogenesis and oxidative metabolism.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    The optimal dose of resveratrol remains elusive in clinical practice, as insufficient effect of resveratrol treatment has been reported in some studies.

    “Despite the array of studies demonstrating beneficial effects of resveratrol in metabolic disorders, optimal dose of resveratrol remains elusive in clinical practice, as insufficient effect of resveratrol treatment has been reported in some studies [90].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [90] Huang C-C, Liu C-C, Tsao J-P, Hsu C-L, Cheng I-S. Effects of oral resveratrol supplementation on glycogen replenishment and mitochondria biogenesis in exercised human skeletal muscle. Nutrients. 2020;12:3721. https://doi.org/10.3390/nu12123721. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Mice that received 40% fat from fish oil for six weeks exhibited high metabolic efficiency and increased respiratory capacity associated with increased gene expression levels of PGC1α/β, citrate synthase enzyme activity, and mitochondrial content.

    “Mice that received 40% fat from fish oil for six weeks of the study period had not only exhibit high metabolic efficiency, but also showed an increased respiratory capacity associated with the increase in gene expression levels of PGC1α/β, and citrate synthase enzyme activity, mitochondrial content [91].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [91] Cavaliere G, et al. Polyunsaturated fatty acids attenuate diet induced obesity and insulin resistance, modulating mitochondrial respiratory uncoupling in rat skeletal muscle. PLoS ONE. 2016;11: e0149033. https://doi.org/10.1371/journal.pone.0149033. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    A human cell line study reported that omega-3 treatment significantly induced both glycolytic and oxidative metabolism and increased mitochondrial content.

    “Similarly, a human cell line study also reported that omega-3 treatment significantly induced both glycolytic and oxidative metabolism and increased mitochondrial content [92].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [92] Vaughan RA, Garcia-Smith R, Bisoffi M, Conn CA, Trujillo KA. Conjugated linoleic acid or omega 3 fatty acids increase mitochondrial biosynthesis and metabolism in skeletal muscle cells. Lipids Health Dis. 2012;11:142. https://doi.org/10.1186/1476-511X-11-142. source

      Not checked in the free run.

60 of 60

  • The paper relies on this without support.

    Impairment of mitochondria induced by obesity is a key factor contributing to the negative effects on skeletal muscle associated with obesity.

    “There is evidence suggesting that the impairment of mitochondria, induced by obesity, is a key factor contributing to the negative effects on skeletal muscle associated with obesity.”
1 of 1

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?

  • Improved mitochondrial efficiency has been observed, but prolonged caloric restriction may reduce mitochondrial biogenesis and oxidative capacity, compromising muscle function even if absolute mass loss is modest.

    “Improved mitochondrial efficiency has been observed, but prolonged caloric restriction may reduce mitochondrial biogenesis and oxidative capacity, compromising muscle function even if absolute mass loss is modest [35].”

    From Muscle loss and GLP-1R agonists use (2025) · cites this paper as [35]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Mfn2 study described as involving mice rather than rat muscle cells

    Minor

    The text attributes a finding in Mfn2-deficient mice to reference 47, whose title identifies its subject as rat skeletal muscle cells.

  • High-fat feeding study described as both long-term and short-term

    Minor

    The text cites reference 27 as evidence about long-term high-fat diet consumption, but that reference's title identifies its intervention as short-term high-fat feeding.

  • Fish-oil study described as using mice rather than rats

    Minor

    The text describes the animals in reference 91 as mice, while the cited reference's title identifies rat skeletal muscle.

3 of 3

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Authors
Jun, L., Tao, Y.-X., Geetha, T., & Babu, J. R.
Affiliations
Auburn University (US)
Corresponding author
Babu, Jeganathan Ramesh
ORCID
Venue
Current Nutrition Reports
Publisher
Springer Science and Business Media LLC
Published
2024-07-08
Volume
13
Issue
3
Pages
500-515
ISSN
2161-3311 (ISSN-L)
DOI
10.1007/s13668-024-00555-7
PMC
PMC11327216
OpenAlex
W4400421862
Semantic Scholar
8ba98acb32f450df4517659cd67314cb0aba9a8f
Cited by
27
References
98
Citations by year
2026: 16 · 2025: 11
FWCI
1.10
Type
journal article
Language
en
Open access
Licence
Locations
  • Current Nutrition Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Auburn University
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
mitochondrial dysfunction, skeletal muscle, obesity, caloric restriction, mitochondrial biogenesis, mitochondrial dynamics, mitochondrial quality control, omega-3 fatty acids, resveratrol, dietary compounds, mitochondrial adaptation
MeSH terms
Resveratrol, Adaptation, Physiological, Animals, Diet, Energy Metabolism, Humans, Mitochondria, Mitochondria, Muscle, Obesity, Fatty Acids, Omega-3, Muscle, Skeletal, Caloric Restriction

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Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-06.

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