Mitochondrial fat oxidation is essential for lipid-induced inflammation in skeletal muscle in mice
Open accessAbstract
Inflammation, lipotoxicity and mitochondrial dysfunction have been implicated in the pathogenesis of obesity-induced insulin resistance and type 2 diabetes. However, how these factors are intertwined in the development of obesity/insulin resistance remains unclear. Here, we examine the role of mitochondrial fat oxidation on lipid-induced inflammation in skeletal muscle. We used skeletal muscle-specific Cpt1b knockout mouse model where the inhibition of mitochondrial fatty acid oxidation results in accumulation of lipid metabolites in muscle and elevated circulating free fatty acids. Gene expression of pro-inflammatory cytokines, chemokines, and cytokine- and members of TLR-signalling pathways were decreased in Cpt1b m−/− muscle. Inflammatory signalling pathways were not activated when evaluated by multiplex and immunoblot analysis. In addition, the inflammatory response to fatty acids was reduced in primary muscle cells derived from Cpt1b m−/− mice. Gene expression of Cd11c , the M1 macrophage marker, was decreased; while Cd206 , the M2 macrophage marker, was increased in skeletal muscle of Cpt1b m−/− mice. Finally, expression of pro-inflammatory markers was decreased in white adipose tissue of Cpt1b m−/− mice. We show that the inflammatory response elicited by elevated intracellular lipids in skeletal muscle is repressed in Cpt1b m−/− mice, strongly supporting the hypothesis that mitochondrial processing of fatty acids is essential for the lipid-induction of inflammation in muscle.
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In carnitine palmitoyltransferase 1B knockout mice, intramyocellular lipid accumulation may not directly induce insulin resistance, but the animals exhibited muscle injury, disrupted metabolism and functional impairment that were partially ameliorated by a low-fat diet.
“A set of interesting experiments in transgenic mice (carnitine palmitoyltransferase 1B knockout) have suggested that IMCL accumulation may not directly induce insulin-resistance, but even these animals’ exhibited markers of muscle injury, disrupted metabolism and functional impairment, which were partially ameliorated by a low-fat diet [67–69].”
From Targeting Intramyocellular Lipids to Improve Aging Muscle Function (2025) · cites this paper as [67]
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- Authors
- Warfel, J. D., Bermudez, E. M., Mendoza, T. M., Ghosh, S., Zhang, J., Elks, C. M., Mynatt, R., & Vandanmagsar, B.
- Affiliations
- Pennington Biomedical Research Center (US)
- Corresponding author
- Vandanmagsar, Bolormaa
- Venue
- Scientific Reports
- Published
- 2016-11-28
- Volume
- 6
- Issue
- 1
- Pages
- 37941-37941
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5124994
- OpenAlex
- W2558537355
- Cited by
- 50
- References
- 76
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 8 · 2023: 2 · 2022: 10 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 3
- FWCI
- 3.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion, cc-by)
- Funders
- National Institutes of Health (NIH 2P30DK072476, DK072476)
- Nutrition Obesity Research Center, University of North Carolina (DK072476, 2P30-DK072476-11A1, 2P30‐DK072476)
- National Institute of General Medical Sciences (P20GM103528, P30GM118430)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK089641, R01DK098687, K01DK106307, T32DK064584, P30DK072476)
- National Center for Research Resources (P20RR021945)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- mitochondrial fatty acid oxidation, CPT1B, skeletal muscle, lipotoxicity, mitochondrial dysfunction, obesity, insulin resistance, type 2 diabetes, inflammatory cytokines, Toll-like receptor signaling, macrophage polarization, M1/M2 macrophages, white adipose tissue, free fatty acids, intracellular lipid accumulation
- MeSH terms
- Animals, Carnitine O-Palmitoyltransferase, Fatty Acids, Gene Expression Regulation, Male, Mitochondria, Muscle, Myositis, Oxidation-Reduction, Signal Transduction, Panniculitis, Cytokines, Mice, Knockout, Muscle, Skeletal, Muscle Fibers, Skeletal, Lipid Metabolism, STAT3 Transcription Factor, Toll-Like Receptors, Diet, High-Fat
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