Different effects of oleate vs. palmitate on mitochondrial function, apoptosis, and insulin signaling in L6 skeletal muscle cells: role of oxidative stress
Open accessAbstract
The type of free fatty acids (FFAs), saturated or unsaturated, is critical in the development of insulin resistance (IR), since the degree of saturation correlates with IR. We compared the effects of the saturated FFA palmitate, the unsaturated FFA oleate, and a mixture of each on the production of mitochondrial reactive oxygen species (mtROS), mitochondrial DNA (mtDNA) damage, mitochondrial function, apoptosis, and insulin-signaling pathway in skeletal muscle cells. Only palmitate caused a significant increase of mtROS production, which correlated with concomitant mtDNA damage, mitochondrial dysfunction, induction of JNK, apoptosis, and inhibition of insulin signaling. Blocking de novo synthesis of ceramide abolished the effects of palmitate on mtROS production, viability, and insulin signaling. Oleate alone did not cause mtROS generation and mtDNA damage, and its addition to palmitate prevented palmitate-induced mtDNA damage, increased total ATP levels and cell viability, and prevented palmitate-induced apoptosis and inhibition of insulin-stimulated Akt (Ser 473 ) phosphorylation. The peroxisome proliferator activator receptor-γ coactivator 1α (PGC-1α) protein level and promoter activity were decreased at concentrations of palmitate ≥0.5 mM, whereas addition of oleate increased both PGC-1α level and promoter activity. Expression of the mitochondrial transcription factor (TFAM) was significantly diminished after palmitate but not oleate treatment. Addition of the ROS scavenger, N-acetylcystein (NAC), to palmitate restored both the expression and promoter activity of PGC-1α as well as TFAM expression. We propose that 1) mtROS generation is the initial event in the induction of mitochondrial dysfunction and consequent apoptosis and the inhibition of insulin signaling and that 2) oleate ameliorates palmitate-induced mitochondrial dysfunction and thus may contribute to the prevention of palmitate-induced IR.
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Palmitic acid affects mitochondrial biogenesis by decreasing PGC1α protein levels and expression of TFAM in L6 skeletal muscle cells.
“Furthermore, palmitic acid also affected mitochondrial biogenesis by decreasing PGC 1α protein levels and the expression of TFAM in L6 skeletal muscle cells (Yuzefovych et al., 2010).”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Yuzefovych et al., 2010
Exposure to long-chain saturated fatty acids has consequences on mitochondrial health, as demonstrated in the L6 rat cell line in which palmitic acid induced mitochondrial dysfunction associated with increased mtDNA damage, induction of JNK, apoptosis, and insulin resistance, all underlain by increased mitochondrial ROS generation.
“Indeed, the exposure to long-chain saturated fatty acids is not without consequences on mitochondrial health as demonstrated in the L6 rat cell line in which palmitic acid, the main long-chain saturated fatty acid in the Western diet, induced mitochondrial dysfunction associated with increased mtDNA damage, induction of c-Jun N-terminal kinases (JNK), apoptosis, and insulin resistance all under”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Yuzefovych et al., 2010
Mitochondrial fuel overload increases production of reactive oxygen species (ROS).
“Mitochondrial fuel overload also increases production of reactive oxygen species (ROS) [19, 20] that may serve to trigger or prime mechanisms that not only induce, but also sustain the loss in mitochondrial function.”
From Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading (2019) · cites this paper as [20]
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- Authors
- Yuzefovych, L., Wilson, G., & Rachek, L.
- Affiliations
- University of South Alabama (US)
- Corresponding author
- Rachek, Lyudmila
- ORCID
- Rachek, Lyudmila
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2010-12
- Volume
- 299
- Issue
- 6
- Pages
- E1096-E1105
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- PMC
- PMC3006254
- OpenAlex
- W2099492526
- Cited by
- 280
- References
- 53
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 13 · 2023: 12 · 2022: 6 · 2021: 8 · 2020: 23 · 2019: 18 · 2018: 19 · 2017: 24 · 2016: 13 · 2015: 25 · 2014: 35 · 2013: 27 · 2012: 22
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-073808, R01DK073808)
- National Institute of Environmental Health Sciences (R01ES003456, ES 03456)
- 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 › Metabolism, Diabetes, and Cancer
- Keywords
- oleate, palmitate, free fatty acids, insulin resistance, mitochondrial reactive oxygen species, mitochondrial DNA damage, mitochondrial dysfunction, apoptosis, insulin signaling, Akt phosphorylation, ceramide, PGC-1α, TFAM, skeletal muscle cells, N-acetylcysteine, oxidative stress
- MeSH terms
- Analysis of Variance, Animals, Cell Count, Cell Line, Cell Survival, Cells, Cultured, Insulin, Insulin Resistance, Mitochondria, Nitric Oxide, Blotting, Western, Signal Transduction, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Muscle Fibers, Skeletal, Oleic Acid, Palmitic Acid, Rats
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