ArticleMetabolism: clinical and experimental2012
Inducible nitric oxide synthase deficiency ameliorates skeletal muscle insulin resistance but does not alter unexpected lower blood glucose levels after burn injury in C57BL/6 mice.
Article in Metabolism: clinical and experimental, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
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- Bioisosteric Replacement in the Search for Biologically Active Compounds: Design, Synthesis and Anti-Inflammatory Activity of Novel [1,2,4]triazino[2,3-c]quinazolines.Pharmaceuticals (Basel, Switzerland) · 2024Article
- [A case of multiple difficult illnesses in a patient with extremely severe burn complicated with type 2 diabetes].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Insulin signaling in skeletal muscle during inflammation and/or immobilisation.Intensive care medicine experimental · 2023Article
- Farnesysltransferase Inhibitor Prevents Burn Injury-Induced Metabolome Changes in Muscle.Metabolites · 2022Article
- Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021Review
- Supplementation with nitrate only modestly affects lipid and glucose metabolism in genetic and dietary-induced murine models of obesity.Journal of clinical biochemistry and nutrition · 2020Article
- Coenzyme Q10 protects against burn-induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle.FEBS open bio · 2019Article
- Inducible satellite cell depletion attenuates skeletal muscle regrowth following a scald-burn injury.The Journal of physiology · 2017Article
- Burn-induced muscle metabolic derangements and mitochondrial dysfunction are associated with activation of HIF-1α and mTORC1: Role of protein farnesylation.Scientific reports · 2017Article
- Article
- miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1.International journal of biological sciences · 2016Article
- Temporal study following burn injury in young rats is associated with skeletal muscle atrophy, inflammation and altered myogenic regulatory factors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- Voluntary Exercise Can Ameliorate Insulin Resistance by Reducing iNOS-Mediated S-Nitrosylation of Akt in the Liver in Obese Rats.PloS one · 2015Article
- Role of protein farnesylation in burn-induced metabolic derangements and insulin resistance in mouse skeletal muscle.PloS one · 2015Article
- Parallel universes of Black Six biology.Biology direct · 2014Article
- iNOS inhibitor, L-NIL, reverses burn-induced glycogen synthase kinase-3β activation in skeletal muscle of rats.Metabolism: clinical and experimental · 2013Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Burn injury is associated with inflammatory responses and metabolic alterations including insulin resistance. Impaired insulin receptor substrate-1 (IRS-1)-mediated insulin signal transduction is a major component of insulin resistance in skeletal muscle following burn injury. To further investigate molecular mechanisms that underlie burn injury-induced insulin resistance, we study a role of inducible nitric oxide synthase (iNOS), a major mediator of inflammation, on burn-induced muscle insulin resistance in iNOS-deficient mice. Full-thickness third-degree burn injury comprising 12% of total body surface area was produced in wild-type and iNOS-deficient C57BL/6 mice. Insulin-stimulated activation (phosphorylation) of IR, IRS-1, and Akt was assessed by immunoblotting and immunoprecipitation. Insulin-stimulated glucose uptake by skeletal muscle was evaluated ex vivo. Burn injury caused induction of iNOS in skeletal muscle of wild-type mice. The increase of iNOS expression paralleled the increase of insulin resistance, as evidenced by decreased tyrosine phosphorylation of IR and IRS-1, IRS-1 expression, insulin-stimulated activation of phosphatidylinositol 3-kinase and Akt/PKB, and insulin-stimulated glucose uptake in mouse skeletal muscle. The absence of iNOS in genetically engineered mice significantly lessened burn injury-induced insulin resistance in skeletal muscle. In wild-type mice, insulin tolerance test revealed whole-body insulin resistance in burned mice compared with sham-burned controls. This effect was reversed by iNOS deficiency. Unexpectedly, however, blood glucose levels were depressed in both wild-type and iNOS-deficient mice after burn injury. Gene disruption of iNOS ameliorated the effect of burn on IRS-1-mediated insulin signaling in skeletal muscle of mice. These findings indicate that iNOS plays a significant role in burn injury-induced skeletal muscle insulin resistance.
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