ArticleBioscience reports2012
Mitochondrial dysfunction in insulin resistance: differential contributions of chronic insulin and saturated fatty acid exposure in muscle cells.
Article in Bioscience reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 3 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Pooled it
- Systematic review and Meta-analysis of acupuncture and acupoint catgut embedding for the treatment of abdominal obesity.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Pooled it
- Identification of novel type 2 diabetes candidate genes involved in the crosstalk between the mitochondrial and the insulin signaling systems.PLoS genetics · 2012Pooled it
- Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026Review
- Molecular pathways, tissue-specific roles, and therapeutic opportunities in mitochondrial resilience-based strategies for insulin resistance.Frontiers in clinical diabetes and healthcare · 2026Review
- Muscle Insulin Resistance Elicits Muscle Atrophy in Obesity.Current obesity reports · 2025Review
- High-fat diet causes mitochondrial damage and downregulation of mitofusin-2 and optic atrophy-1 in multiple organs.Journal of clinical biochemistry and nutrition · 2023Article
- Mitochondrial DNA Polymorphism in HV1 and HV2 Regions and 12S rDNA in Perimenopausal Hypertensive Women.Biomedicines · 2023Article
- CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells.International journal of molecular sciences · 2023Article
- Elevated LDL-C, high blood pressure, and low peakFrontiers in molecular biosciences · 2023Article
- Multi-omics study identifies novel signatures of DNA/RNA, amino acid, peptide, and lipid metabolism by simulated diabetes on coronary endothelial cells.Scientific reports · 2022Article
- Effects of Red Rice Bran Extract on High-Fat Diet-Induced Obesity and Insulin Resistance in Mice.Preventive nutrition and food science · 2022Article
- Hypoxia-induced HIF1α activation regulates small extracellular vesicle release in human embryonic kidney cells.Scientific reports · 2022Article
- Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet.International journal of molecular sciences · 2020Article
- Metabolic implications of organelle-mitochondria communication.EMBO reports · 2019Review
- RAGE-NF-κB-PPARγ Signaling is Involved in AGEs-Induced Upregulation of Amyloid-β Influx Transport in an In Vitro BBB Model.Neurotoxicity research · 2018Article
- Cbl downregulation increases RBP4 expression in adipocytes of female mice.The Journal of endocrinology · 2018Article
- Metabolomics allows the discrimination of the pathophysiological relevance of hyperinsulinism in obese prepubertal children.International journal of obesity (2005) · 2017Article
- FOXO1 and GSK-3β Are Main Targets of Insulin-Mediated Myogenesis in C2C12 Muscle Cells.PloS one · 2016Article
- Unraveling biochemical pathways affected by mitochondrial dysfunctions using metabolomic approaches.Metabolites · 2014Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction has been associated with insulin resistance, obesity and diabetes. Hyperinsulinaemia and hyperlipidaemia are hallmarks of the insulin-resistant state. We sought to determine the contributions of high insulin and saturated fatty acid exposure to mitochondrial function and biogenesis in cultured myocytes. Differentiated C2C12 myotubes were left untreated or exposed to chronic high insulin or high palmitate. Mitochondrial function was determined assessing: oxygen consumption, mitochondrial membrane potential, ATP content and ROS (reactive oxygen species) production. We also determined the expression of several mitochondrial genes. Chronic insulin treatment of myotubes caused insulin resistance with reduced PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) signalling. Insulin treatment increased oxygen consumption but reduced mitochondrial membrane potential and ROS production. ATP cellular levels were maintained through an increased glycolytic rate. The expression of mitochondrial OXPHOS (oxidative phosphorylation) subunits or Mfn-2 (mitofusin 2) were not significantly altered in comparison with untreated cells, whereas expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α) and UCPs (uncoupling proteins) were reduced. In contrast, saturated fatty acid exposure caused insulin resistance, reducing PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) activation while increasing activation of stress kinases JNK (c-Jun N-terminal kinase) and p38. Fatty acids reduced oxygen consumption and mitochondrial membrane potential while up-regulating the expression of mitochondrial ETC (electron chain complex) protein subunits and UCP proteins. Mfn-2 expression was not modified by palmitate. Palmitate-treated cells also showed a reduced glycolytic rate. Taken together, our findings indicate that chronic insulin and fatty acid-induced insulin resistance differentially affect mitochondrial function. In both conditions, cells were able to maintain ATP levels despite the loss of membrane potential; however, different protein expression suggests different adaptation mechanisms.
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