Cited by 277Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressMetabolism, Diabetes, and Cancer

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S-Nitrosation of the Insulin Receptor, Insulin Receptor Substrate 1, and Protein Kinase B/Akt

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Carvalho-Filho, Marco A., Ueno, Mirian, Hirabara, Sandro M., Seabra, Amedea B., Carvalheira, José B.C., de Oliveira, Marcelo G., Velloso, Lício A., Curi, Rui, Saad, Mario J.A.·2005·Diabetes

DOI 10.2337/diabetes.54.4.959

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Abstract

Evidence demonstrates that exogenous nitric oxide (NO) and the NO produced by inducible nitric oxide synthase (iNOS) can induce insulin resistance in muscle. Here, we investigated whether this insulin resistance could be mediated by S-nitrosation of proteins involved in early steps of the insulin signal transduction pathway. Exogenous NO donated by S-nitrosoglutathione (GSNO) induced in vitro and in vivo S-nitrosation of the insulin receptor beta subunit (IRbeta) and protein kinase B/Akt (Akt) and reduced their kinase activity in muscle. Insulin receptor substrate (IRS)-1 was also rapidly S-nitrosated, and its expression was reduced after chronic GSNO treatment. In two distinct models of insulin resistance associated with enhanced iNOS expression-diet-induced obesity and the ob/ob diabetic mice-we observed enhanced S-nitrosation of IRbeta/IRS-1 and Akt in muscle. Reversal of S-nitrosation of these proteins by reducing iNOS expression yielded an improvement in insulin action in both animal models. Thus, S-nitrosation of proteins involved in insulin signal transduction is a novel molecular mechanism of iNOS-induced insulin resistance.

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[RETRACTION]Translational research into gut microbiota: new horizons in obesity treatment
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Retracted

Authors: Carvalho-Filho, M. A., Ueno, M., Hirabara, S. M., Seabra, A. B., Carvalheira, J. B. C., de Oliveira, M. G., Velloso, L. A., Curi, R., & Saad, M. J. A.
Affiliations: Department of Internal Medicine, State University of Campinas, UNICAMP, Campinas, Brazil
Universidade Estadual de Campinas (UNICAMP) (BR)
Universidade de São Paulo (BR)
Chemistry Institute, State University of Campinas, UNICAMP, Campinas, Brazil
ORCID: Hirabara, Sandro M.
Seabra, Amedea B.
Curi, Rui
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2005-04-01
Volume: 54
Issue: 4
Pages: 959-967
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/diabetes.54.4.959
OpenAlex: W2144153442
Cited by: 277
References: 53
Citations by year: 2026: 8 · 2025: 7 · 2024: 3 · 2023: 5 · 2022: 15 · 2021: 5 · 2020: 13 · 2019: 9 · 2018: 12 · 2017: 13 · 2016: 13 · 2015: 22 · 2014: 13 · 2013: 18 · 2012: 25
FWCI: 7.59
Type: journal article
Language: en
Update notices: expression_of_concern (2023-10-23)
Open access: bronze
doi.org
Locations: Diabetes (publishedVersion)
PubMed (publishedVersion)
University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: S-nitrosylation, insulin resistance, insulin receptor beta-subunit, IRS-1, Akt/protein kinase B, nitric oxide, inducible nitric oxide synthase, S-nitrosoglutathione, insulin signaling, skeletal muscle, diet-induced obesity, ob/ob mice, kinase activity
MeSH terms: Rosiglitazone, Animals, Glutathione, Insulin, Insulin Resistance, Male, Nitric Oxide, Nitro Compounds, Obesity, Phosphoproteins, Protein Processing, Post-Translational, Proto-Oncogene Proteins, Receptor, Insulin, Nitrosation, Mice, Inbred NOD, Rats, Wistar, Protein Serine-Threonine Kinases, Muscle, Skeletal, Thiazolidinediones, Proto-Oncogene Proteins c-akt, Mice, Rats, Insulin Receptor Substrate Proteins

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S-Nitrosation of the Insulin Receptor, Insulin Receptor Substrate 1, and Protein Kinase B/Akt

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