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Cited by 24Immunotoxicology and immune responsesAnimal testing and alternativesDrug-Induced Hepatotoxicity and Protection

The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.

Biomarker evaluation of skeletal muscle toxicity following clofibrate administration in rats

Open access
Bodié, Karen, Buck, Wayne R., Pieh, Julia, Liguori, Michael J., Popp, Andreas·2016·Experimental and Toxicologic Pathology
DOI 10.1016/j.etp.2016.03.001
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Abstract

The use of sensitive biomarkers to monitor skeletal muscle toxicity in preclinical toxicity studies is important for the risk assessment in humans during the development of a novel compound. Skeletal muscle toxicity in Sprague Dawley Rats was induced with clofibrate at different dose levels for 7 days to compare standard clinical pathology assays with novel skeletal muscle and cardiac muscle biomarkers, gene expression and histopathological changes. The standard clinical pathology assays aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) enzyme activity were compared to novel biomarkers fatty acid binding protein 3 (Fabp3), myosin light chain 3 (Myl3), muscular isoform of CK immunoreactivity (three isoforms CKBB, CKMM, CKMB), parvalbumin (Prv), skeletal troponin I (sTnI), cardiac troponin T (cTnT), cardiac troponin I (cTnI), CKMM, and myoglobin (Myo). The biomarker elevations were correlated to histopathological findings detected in several muscles and gene expression changes. Clofibrate predominantly induced skeletal muscle toxicity of type I fibers of low magnitude. Useful biomarkers for skeletal muscle toxicity were AST, Fabp3, Myl3, (CKMB) and sTnI. Measurements of CK enzyme activity by a standard clinical assay were not useful for monitoring clofibrate-induced skeletal muscle toxicity in the rat at the doses used in this study.

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Crossref · 10.1016/j.etp.2016.03.001

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  • Upregulation of beta-oxidation genes by FEN results in a metabolic transition of energy fuel from glucose to fatty acid that may be a cause of FEN-induced muscle toxicity.

    “This upregulation results in a metabolic transition of the energy fuel from glucose to fatty acid that may be a cause of FEN-induced muscle toxicity.”

    From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as Bodie et al. 2016

    The Introduction links fenofibrate’s effects on type I muscle fibers with increased fatty-acid uptake and beta-oxidation. But the study tested clofibrate, not fenofibrate; its Gene expression and Discussion sections do not show that fenofibrate upregulates beta-oxidation genes, shifts muscle fuel use from glucose to fatty acids, or causes toxicity through that shift. No page numbers are available in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • FEN has a selective effect on type I muscle fibers via upregulation of genes of beta-oxidation of fatty acid.

    “FEN has a selective effect on type I muscle fibers via upregulation of genes of beta-oxidation of fatty acid.”

    From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as Bodie et al. 2016

    The Introduction (page not specified in our copy) reports that fenofibrate selectively affects type I muscle fibers and links this to increased fatty-acid uptake and beta-oxidation. It does not say that upregulation of beta-oxidation genes mediates that effect. The gene-expression results in §3.5 concern clofibrate, not fenofibrate, and describe dysregulated genes rather than that proposed mechanism. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Skeletal muscle toxicity induced by fibrate might be caused by inhibition of mitochondrial respiratory complex I, leading to impaired mitochondrial functions.

    “Previous research has shown that skeletal muscle toxicity induced by fibrate might be caused by inhibition of the mitochondrial respiratory complex I, leading to impaired mitochondrial functions”

    From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as Bodie et al. 2016

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Research works printed but not linked: 2

  1. 1989, vol. 617, 622
  2. Jackson, 2007, vol. 298, 223

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Metadata

Authors
Bodié, K., Buck, W. R., Pieh, J., Liguori, M. J., & Popp, A.
Affiliations
  • AbbVie (Germany) (DE)
  • AbbVie (United States) (US)
Corresponding author
Bodié, Karen
ORCID
Buck, Wayne R.
Venue
Experimental and Toxicologic Pathology
Publisher
Elsevier BV
Published
2016-05
Volume
68
Issue
5
Pages
289-299
ISSN
0940-2993 (ISSN-L)
DOI
10.1016/j.etp.2016.03.001
OpenAlex
W2304754516
Cited by
24
References
24
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 2 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 2 · 2017: 4
FWCI
1.81
Type
journal article
Language
en
Open access
Licence
Locations
  • Experimental and Toxicologic Pathology (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
Cordula Geschwill and Katrin Goetzke for the immunohistochmical stainings
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
  • Health Sciences › Veterinary › Small Animals › Animal testing and alternatives
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
clofibrate, skeletal muscle toxicity, biomarkers, fatty acid binding protein 3, MYL3, creatine kinase isoforms, creatine kinase MM, cardiac troponin T, parvalbumin, myoglobin, type I muscle fibers, hepatotoxicity, gene expression, histopathology
MeSH terms
Fatty Acid Binding Protein 3, Alanine Transaminase, Animals, Hypolipidemic Agents, Aspartate Aminotransferases, Clofibrate, Creatine Kinase, Heart, Male, Myocardium, Myoglobin, Parvalbumins, Biomarkers, Rats, Sprague-Dawley, Muscle, Skeletal, Myosin Light Chains, Troponin C, Troponin I, Gene Expression Profiling, Fatty Acid-Binding Proteins, Rats

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