Cited by 159Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes and associated disorders

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Roles of insulin resistance and beta-cell dysfunction in dexamethasone-induced diabetes.

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Ogawa, A, Johnson, J H, Ohneda, M, McAllister, C T, Inman, L, Alam, T, Unger, R H·1992·Journal of Clinical Investigation

DOI 10.1172/jci115886PMC PMC443126

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Abstract

The roles of insulin resistance and beta-cell dysfunction in glucocorticoid-induced diabetes were determined in Wistar and Zucker (fa/fa) rats. All Wistar rats treated with 5 mg/kg per d of dexamethasone for 24 d exhibited increased beta-cell mass and basal and arginine-stimulated insulin secretion, indicating insulin resistance, but only 16% became diabetic. The insulin response to 20 mM glucose was normal in the perfused pancreas of all normoglycemic dexamethasone-treated rats but absent in every diabetic rat. Immunostainable high Km beta-cell transporter, GLUT-2, was present in approximately 100% of beta-cells of normoglycemic rats, but in only 25% of beta cells of diabetic rats. GLUT-2 mRNA was not reduced. All Zucker (fa/fa) rats treated with 0.2-0.4 mg/kg per d of dexamethasone for 24 d became diabetic and glucose-stimulated insulin secretion was absent in all. High Km glucose transport in islets was 50% below nondiabetic controls. Only 25% of beta cells of diabetic rats were GLUT-2-positive compared with approximately 100% in controls. Total pancreatic GLUT-2 mRNA was increased twofold suggesting a posttranscriptional abnormality. We conclude that dexamethasone induces insulin resistance, whether or not it induces hyperglycemia. Whenever hyperglycemia is present, GLUT-2-positive beta cells are reduced, high Km glucose transport into beta cells is attenuated and the insulin response to glucose is absent.

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Authors: Ogawa, A., Johnson, J. H., Ohneda, M., McAllister, C. T., Inman, L., Alam, T., & Unger, R. H.
Affiliations: The University of Texas Southwestern Medical Center (US)
Veterans Health Administration (US)
ORCID: Johnson, J H
McAllister, C T
Alam, T
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1992-08-01
Volume: 90
Issue: 2
Pages: 497-504
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci115886
PMC: PMC443126
OpenAlex: W1983709201
Cited by: 159
References: 19
Citations by year: 2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 7 · 2020: 3 · 2019: 4 · 2018: 6 · 2017: 4 · 2016: 9 · 2015: 4 · 2014: 6 · 2013: 5 · 2012: 5
FWCI: 7.33
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5p01dk042582-04)
National Institute of Diabetes and Digestive and Kidney Diseases (DK-02700-31, 1-P01-DK42582-01)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords: glucocorticoid-induced diabetes, dexamethasone, insulin resistance, beta-cell dysfunction, GLUT2, glucose-stimulated insulin secretion, beta-cell mass, Zucker fatty rats, pancreatic islets, hyperglycemia
MeSH terms: Animals, Biological Transport, Dexamethasone, Diabetes Mellitus, Experimental, Fluorescent Antibody Technique, Glucose, Insulin, Insulin Resistance, Islets of Langerhans, Monosaccharide Transport Proteins, RNA, Messenger, Secretory Rate, Gene Expression, Rats

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Roles of insulin resistance and beta-cell dysfunction in dexamethasone-induced diabetes.

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