ArticleEndocrine2003
Regulation of insulin receptor substrate-2 tyrosine phosphorylation in animal models of insulin resistance.
Article in Endocrine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial.Diabetologia · 2011Trial
- Glucocorticoid-induced diabetes mellitus: mechanisms, risk factors, and clinical pathways with insights from autoimmune rheumatic diseases.Rheumatology international · 2026Review
- ProteinMetabolites · 2022Review
- Fresh insights into glucocorticoid-induced diabetes mellitus and new therapeutic directions.Nature reviews. Endocrinology · 2022Review
- Potential Roles of Glucagon-Like Peptide-1 and Its Analogues in Dementia Targeting Impaired Insulin Secretion and Neurodegeneration.Degenerative neurological and neuromuscular disease · 2022Review
- The Role of Insulin Resistance and Protein O-GlcNAcylation in Neurodegeneration.Frontiers in neuroscience · 2019Review
- Regulation of hepatic NaMolecular and cellular biochemistry · 2018Article
- Insulin regulates nitric oxide production in the kidney collecting duct cells.The Journal of biological chemistry · 2015Article
- Central amygdala nucleus (Ce) gene expression linked to increased trait-like Ce metabolism and anxious temperament in young primates.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Reduction of insulin signalling pathway IRS-1/IRS-2/AKT/mTOR and decrease of epithelial cell proliferation in the prostate of glucocorticoid-treated rats.International journal of experimental pathology · 2012Article
- 11beta-hydroxysteroid dehydrogenase type 1 regulates glucocorticoid-induced insulin resistance in skeletal muscle.Diabetes · 2009Article
- Article
- Glucocorticoid modulation of insulin signaling in human subcutaneous adipose tissue.The Journal of clinical endocrinology and metabolism · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin induces a wide variety of growth and metabolic responses in many cell types. These actions are initiated by insulin binding to its receptor and involve a series of alternative and complementary pathways created by the multiple substrates of the insulin receptor (insulin receptor substrates [IRSs]). We investigated IRS-1 and IRS-2 tyrosine phosphorylation; their association with phosphatidylinositol-3-OH kinase (PI3-K); and the phosphorylation of Akt, a serine-threonine kinase situated downstream of PI3-K, in liver and muscle of two animal models of insulin resistance: epinephrine- or dexamethasone-treated rats. We used in vivo insulin infusion followed by tissue extraction, immunoprecipitation, and immunoblotting. IRS-1 and IRS-2 protein expression did not change in liver and muscle of the epinephrine- treated rats, but in dexamethasone-treated rats IRS-1 presented an increase in liver and a decrease in muscle tissue. PI3-K and Akt protein expression did not change in liver or muscle of the two animal models of insulin resistance. There was a downregulation in insulin- induced IRS-1 and IRS-2 tyrosine phosphorylation and association with PI3-K in both models of insulin resistance. In parallel, insulin-induced Akt phosphorylation was reduced in both tissues of epinephrine-treated rats, and in liver but not in muscle of dexamethasonetreated rats. The reduction in insulin-induced Akt phosphorylation may help to explain the insulin resistance in liver and muscle of epinephrine-treated rats and in the liver of dexamethasone-treated rats.
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