ArticlePloS one2014
Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 63 citations in OpenAlex.
- Hypercortisolism: An Under-Recognised Pathway Linked to Multi-System Complications.Diabetes, obesity & metabolism · 2026Review
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- Effects of Anterior Pituitary Adenomas' Hormones on Glucose Metabolism and Its Clinical Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Review
- The difference between steroid diabetes mellitus and type 2 diabetes mellitus: a whole-bodyActa diabetologica · 2020Article
- Glucose metabolism in Cushing's syndrome.Current opinion in endocrinology, diabetes, and obesity · 2020Review
- Glucocorticoid-Induced Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Antioxidant, antihyperglycemic, and antidyslipidemic effects of Brazilian-native fruit extracts in an animal model of insulin resistance.Redox report : communications in free radical research · 2018Article
- Glucose Homeostasis Is Not Affected in a Murine Model of Parkinson's Disease Induced by 6-OHDA.Frontiers in neuroscience · 2018Article
- Effects of chronic dexamethasone administration on hyperglycemia and insulin release in goats.Journal of animal science and biotechnology · 2018Article
- Impact of Fish Oil Supplementation and Interruption of Fructose Ingestion on Glucose and Lipid Homeostasis of Rats Drinking Different Concentrations of Fructose.BioMed research international · 2017Article
- Metabolic effects of prazosin on skeletal muscle insulin resistance in glucocorticoid-treated male rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Impact of Glucocorticoid Excess on Glucose Tolerance: Clinical and Preclinical Evidence.Metabolites · 2016Review
- Neuronostatin acts via GPR107 to increase cAMP-independent PKA phosphorylation and proglucagon mRNA accumulation in pancreatic α-cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Regulation of Glucose Homeostasis by Glucocorticoids.Advances in experimental medicine and biology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid (GC)-based therapies can cause insulin resistance (IR), glucose intolerance, hyperglycemia and, occasionally, overt diabetes. Understanding the mechanisms behind these metabolic disorders could improve the management of glucose homeostasis in patients undergoing GC treatment. For this purpose, adult rats were treated with a daily injection of dexamethasone (1 mg/kg b.w., i.p.) (DEX) or saline as a control for 5 consecutive days. The DEX rats developed IR, augmented glycemia, hyperinsulinemia and hyperglucagonemia. Treatment of the DEX rats with a glucagon receptor antagonist normalized their blood glucose level. The characteristic inhibitory effect of glucose on glucagon secretion was impaired in the islets of the DEX rats, while no direct effects were found on α-cells in islets that were incubated with DEX in vitro. A higher proportion of docked secretory granules was found in the DEX α-cells as well as a trend towards increased α-cell mass. Additionally, insulin secretion in the presence of glucagon was augmented in the islets of the DEX rats, which was most likely due to their higher glucagon receptor content. We also found that the enzyme 11βHSD-1, which participates in GC metabolism, contributed to the insulin hypersecretion in the DEX rats under basal glucose conditions. Altogether, we showed that GC treatment induces hyperglucagonemia, which contributes to an imbalance in glucose homeostasis and compensatory β-cell hypersecretion. This hyperglucagonemia may result from altered α-cell function and, likely, α-cell mass. Additionally, blockage of the glucagon receptor seems to be effective in preventing the elevation in blood glucose levels induced by GC administration.
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