Modulation of insulin receptor, insulin receptor substrate-1, and phosphatidylinositol 3-kinase in liver and muscle of dexamethasone-treated rats.

Saad, M J; Folli, F; Kahn, J A; Kahn, C R

doi:10.1172/jci116803

Cited by 349Metabolism, Diabetes, and CancerAdipokines, Inflammation, and Metabolic DiseasesEstrogen and related hormone effects

Modulation of insulin receptor, insulin receptor substrate-1, and phosphatidylinositol 3-kinase in liver and muscle of dexamethasone-treated rats.

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Saad, M J, Folli, F, Kahn, J A, Kahn, C R·1993·Journal of Clinical Investigation

DOI 10.1172/jci116803PMC PMC288376

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Abstract

Insulin rapidly stimulates tyrosine kinase activity of its receptor resulting in phosphorylation of its cytosolic substrate, insulin receptor substrate-1 (IRS-1), which in turn associates with phosphatidylinositol 3-kinase (PI 3-kinase), thus activating the enzyme. Glucocorticoid treatment is known to produce insulin resistance, but the exact molecular mechanism is unknown. In the present study we have examined the levels and phosphorylation state of the insulin receptor and IRS-1, as well as the association/activation between IRS-1 and PI 3-kinase in the liver and muscle of rats treated with dexamethasone. After dexamethasone treatment (1 mg/kg per d for 5 d), there was no change in insulin receptor concentration in liver of rats as determined by immunoblotting with antibody to the COOH-terminus of the receptor. However, insulin stimulation of receptor autophosphorylation determined by immunoblotting with antiphosphotyrosine antibody was reduced by 46.7 +/- 9.1%. IRS-1 and PI 3-kinase protein levels increased in liver of dexamethasone-treated animals by 73 and 25%, respectively (P < 0.05). By contrast, IRS-1 phosphorylation was decreased by 31.3 +/- 10.9% (P < 0.05), and insulin stimulated PI 3-kinase activity in anti-IRS-1 immunoprecipitates was decreased by 79.5 +/- 11.2% (P < 0.02). In muscle, the changes were less dramatic, and often in opposite direction of those observed in liver. Thus, there was no significant change in insulin receptor level or phosphorylation after dexamethasone treatment. IRS-1 and PI 3-kinase levels were decreased to 38.6 and 65.6%, respectively (P < 0.01 and P < 0.05). IRS-1 phosphorylation showed no significant change in muscle, but insulin-stimulated IRS-1 associated PI 3-kinase was decreased by 41%. Thus, dexamethasone has differential effects on the proteins involved in the early steps in insulin action in liver and muscle. In both tissues, dexamethasone treatment results in a reduction in insulin-stimulated IRS-1-associated P I3-kinase, which may play a role in the pathogenesis of insulin resistance at the cellular level in these animals.

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GCs were shown to interfere with insulin signalling in vitro and in vivo in rodents in liver, adipose tissue and skeletal muscle.
“GCs were shown to interfere with insulin signalling in vitro and in vivo in rodents in liver [38], adipose tissue [39] and skeletal muscle [40].”
From Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial (2011) · cites this paper as [40]
For the liver claim attached to [38], the Abstract and Introduction describe impaired insulin signalling in the liver of dexamethasone-treated rats after insulin stimulation in vivo. The Introduction mentions in vitro findings from earlier studies, but this paper does not establish a liver finding from its own in vitro experiment. The adipose-tissue and skeletal-muscle claims have separate citations. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Dexamethasone-induced insulin resistance does not alter tyrosine phosphorylation of the insulin receptor.
“Dexamethasone-induced insulin resistance does not alter tyrosine phosphorylation of the insulin receptor [18,26]”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [26]
Dexamethasone-induced insulin resistance inhibits insulin-stimulated IRS-1-associated PI 3-kinase activity.
“but inhibits insulin-stimulated IRS-1 associated PI 3-kinase activity [26].”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [26]
A daily intraperitoneal injection of dexamethasone (1.0 mg/kg) for 12 days induces a state of insulin resistance in rats.
“This concentration has previously been reported to induce a state of insulin resistance [16,26].”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [26]
Dexamethasone treatment reduces IRS-1-associated PI 3-kinase activity.
“whereas dexamethasone treatment reduces IRS-1-associated PI 3-kinase activity [26].”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [26]

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Authors: Saad, M. J., Folli, F., Kahn, J. A., & Kahn, C. R.
Affiliations: Joslin Diabetes Center (US)
Brigham and Women's Hospital (US)
ORCID: Folli, F
Kahn, C R
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1993-10-01
Volume: 92
Issue: 4
Pages: 2065-2072
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci116803
PMC: PMC288376
OpenAlex: W1986519087
Cited by: 349
References: 42
Citations by year: 2026: 3 · 2025: 3 · 2024: 5 · 2023: 8 · 2022: 10 · 2021: 9 · 2020: 14 · 2019: 2 · 2018: 11 · 2017: 10 · 2016: 14 · 2015: 9 · 2014: 15 · 2013: 12 · 2012: 12
FWCI: 2.57
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
Funders: Joslin Diabetes Center
Conselho Nacional de Desenvolvimento Científico e Tecnológico
National Institutes of Health (DK 36836)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 33201, DK36836, R01DK033201, P30DK036836)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords: insulin resistance, glucocorticoids, dexamethasone, insulin receptor, IRS-1, phosphatidylinositol 3-kinase, insulin receptor autophosphorylation, IRS-1 phosphorylation, liver, skeletal muscle, insulin signaling, insulin receptor tyrosine kinase, tissue-specific effects, rats, enzyme activity
MeSH terms: Amino Acid Sequence, Animals, Antibodies, Dexamethasone, Insulin, Kinetics, Liver, Male, Molecular Sequence Data, Muscles, Peptides, Phosphoproteins, Phosphorylation, Receptor, Insulin, Tyrosine, Immunoblotting, Phosphotransferases (Alcohol Group Acceptor), Phosphotyrosine, Phosphatidylinositol 3-Kinases, Rats, Insulin Receptor Substrate Proteins

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Modulation of insulin receptor, insulin receptor substrate-1, and phosphatidylinositol 3-kinase in liver and muscle of dexamethasone-treated rats.

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