Role of Glucose Transporters in Glucocorticoid-Induced Insulin Resistance: GLUT4 Isoform in Rat Skeletal Muscle is Not Decreased by Dexamethasone
Abstract
The diabetogenic effects of glucocorticoid excess are due in part to peripheral resistance to insulin. To test the hypothesis that glucocorticoid-induced peripheral insulin resistance might be attributable to a decreased number of glucose transporters, we examined the effects of dexamethasone treatment on the expression of the GLUT4 (insulin regulatable) glucose transporter in skeletal muscle, the major site of insulin-mediated glucose uptake. Dexamethasone treatment of rats (1 mg/day for 1 wk) induced hyperglycemia and hyperinsulinemia. At dosages of either 0.1 or 1 mg/day, insulin-stimulated 2-deoxyglucose uptake in isolated soleus muscle was reduced by ≥ 50%, demonstrating the presence of insulin resistance in skeletal muscle. Immunoblots of crude membranes from deep quadriceps muscle showed that dexamethasone treatment (1 mg/day) increased the amount of GLUT4 protein by 84%. GLUT4 mRNA abundance was similarly increased when expressed per unit RNA but was unchanged when expressed on a DNA basis because the tissue RNA content was decreased by dexamethasone. In contrast to quadriceps, GLUT4 protein concentration in soleus and extensor digitorum longus extracts was not significantly increased by dexamethasone treatment. Because glucocorticoids cause selective atrophy of type IIb muscle fibers, which express relatively less GLUT4 protein, the apparent increase in GLUT4 content in quadriceps muscle from dexamethasone-treated animals may have resulted from inadvertent increased sampling of GLUT4-enriched type I and IIA fibers, caused by a glucocorticoid-induced decrease in the relative mass of the GLUT4-poor type IIb fibers. We conclude that glucocorticoids do not decrease GLUT4 content in skeletal muscle and that glucocorticoid-induced insulin resistance in this tissue is not due to suppression of glucose transporter gene expression.
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Chronic treatment with dexamethasone decreases insulin-stimulated glucose uptake and GLUT4 translocation in skeletal muscle without reducing total GLUT4 content.
“Chronic treatment with the glucocorticoid analogue dexamethasone decreases insulinstimulated glucose uptake and GLUT4 translocation in skeletal muscle without reducing the total content of GLUT4 [16,17].”
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].”
Glucocorticoid treatment increased GLUT4 expression in the fast-twitch epitrochlearis muscles.
“as reported previously [16], glucocorticoid treatment increased GLUT4 expression in the fast-twitch epitrochlearis muscles”
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ResultBerg, R. M. G., & Pedersen, B. K. (2009) · doi:10.1002/9783527628346.ch18
- Authors
- Haber, R. S., & Weinstein, S. P.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1992-06-01
- Volume
- 41
- Issue
- 6
- Pages
- 728-735
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2171420300
- Cited by
- 77
- References
- 0
- Citations by year
- 2025: 1 · 2023: 5 · 2022: 1 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 4
- FWCI
- 1.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k08dk002057-04, 5r01dk041674-03)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-41674, DK-02057)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- glucocorticoid-induced insulin resistance, GLUT4, glucose transporters, dexamethasone, skeletal muscle, soleus muscle, quadriceps, type IIb muscle fibers, muscle fiber atrophy, insulin-stimulated glucose uptake, hyperinsulinemia, hyperglycemia
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Cell Membrane, Deoxyglucose, Dexamethasone, DNA, Feeding Behavior, Insulin, Insulin Resistance, Male, Methylglucosides, Monosaccharide Transport Proteins, Muscles, Rats, Inbred Strains, RNA, Messenger, 3-O-Methylglucose, Rats
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