Acute and 2-week exposure to prednisolone impair different aspects of β-cell function in healthy men
Abstract
OBJECTIVE: Glucocorticoids (GCs), such as prednisolone, are associated with adverse metabolic effects, including glucose intolerance and diabetes. In contrast to the well known GC-induced insulin resistance, the effects of GCs on beta-cell function are less well established. We assessed the acute and short-term effects of prednisolone treatment on beta-cell function in healthy men. RESEARCH DESIGN AND METHODS: A randomised, double-blind, placebo-controlled trial consisting of two protocols was conducted. In protocol 1 (n=6), placebo and a single dose of 75 mg of prednisolone were administered. In protocol 2 (n=23), participants received 30 mg of prednisolone daily or placebo for 15 days. Both empirical and model-based parameters of beta-cell function were calculated from glucose, insulin and C-peptide concentrations obtained during standardised meal tests before and during prednisolone treatment (protocols 1 and 2), and 1 day after cessation of treatment (protocol 2). RESULTS: Seventy-five milligrams of prednisolone acutely increased the area under the postprandial glucose curve (AUC(gluc); P=0.005), and inhibited several parameters of beta-cell function, including AUC(c-pep)/AUC(gluc) ratio (P=0.004), insulinogenic index (P=0.007), glucose sensitivity (P=0.02) and potentiation factor ratio (PFR; P=0.04). A 15-day treatment with prednisolone increased AUC(gluc) (P<0.001), despite augmented C-peptide secretion (P=0.05). beta-cell function parameters were impaired, including the fasting insulin secretory tone (P=0.02) and PFR (P=0.007). CONCLUSIONS: Acute and short-term exposure to prednisolone impairs different aspects of beta-cell function, which contribute to its diabetogenic effects.
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This observation is in line with previous studies reporting large postprandial glucose excursions with only modest changes in fasting glucose levels.
“This observation is in line with previous studies reporting large postprandial glucose excursions with only modest changes in fasting glucose levels [19, 26].”
From Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial (2011) · cites this paper as [19]
The effects of synthetic GCs on pancreatic islets and insulin biosynthesis or release depend on the dose and duration of GCs treatment.
“Several studies proposed that the effects of synthetic GCs on pancreatic islets and insulin biosynthesis or release depend on the dose and duration of GCs treatment (23, 24).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [24]
Steroids increase basal endogenous glucose production and lower insulin sensitivity.
“due to their effect of increasing basal endogenous glucose production and lowering insulin sensitivity.7–9”
In healthy men, acute prednisolone 75 mg/day had an acute inhibitory effect on the β-cell, while longer exposure to 30 mg/day caused fasting and postprandial hyperglycaemia but relative hypoinsulinemia, thought secondary to insufficient compensatory β-cell response.
“In a recent study by van Raalte et al.11 in healthy men, acute treatment with 75 mg/day of prednisolone resulted in an acute inhibitory effect of the â-cell, but longer exposure with a prednisolone dose of 30 mg/day resulted in fasting and postprandial hyperglycaemia but relative hypoinsulinemia, which was thought to be secondary to the insufficient compensatory â-cell response.”
From Twenty‐four‐hour profiles of plasma glucose, insulin, C‐peptide and free fatty acid in subjects with varying degrees of glucose tolerance following short‐term, medium‐dose prednisone (20 mg/day) treatment: evidence for differing effects on insulin secretion and action (2012) · cites this paper as [11]
Animal studies show direct inhibitory effects of glucocorticoids on insulin secretion, and some human studies show adverse effects on β-cell function.
“In addition, animal studies8,9 have demonstrated direct inhibitory effects of GCs on insulin secretion and adverse effects on â-cell function in some human studies.10,11”
From Twenty‐four‐hour profiles of plasma glucose, insulin, C‐peptide and free fatty acid in subjects with varying degrees of glucose tolerance following short‐term, medium‐dose prednisone (20 mg/day) treatment: evidence for differing effects on insulin secretion and action (2012) · cites this paper as [11]
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References 27 · Cited by 170
- Authors
- van Raalte, D. H., Nofrate, V., Bunck, M. C., van Iersel, T., Elassaiss Schaap, J., Nässander, U. K., Heine, R. J., Mari, A., Dokter, W. H. A., & Diamant, M.
- Affiliations
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Venue
- European Journal of Endocrinology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-04
- Volume
- 162
- Issue
- 4
- Pages
- 729-735
- ISSN
- 0804-4643 (ISSN-L)
- 1479-683X
- OpenAlex
- W1974022347
- Cited by
- 170
- References
- 27
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 9 · 2021: 15 · 2020: 13 · 2019: 11 · 2018: 10 · 2017: 9 · 2016: 11 · 2015: 12 · 2014: 13 · 2013: 12 · 2012: 13
- FWCI
- 13.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- prednisolone, glucocorticoids, beta-cell function, insulin secretion, impaired glucose tolerance, diabetogenic effect, C-peptide, insulinogenic index, glucose sensitivity, postprandial blood glucose
- MeSH terms
- Adult, Blood Glucose, C-Peptide, Double-Blind Method, Drug Administration Schedule, Glucocorticoids, Humans, Insulin, Insulin Resistance, Male, Middle Aged, Prednisolone, Postprandial Period, Insulin-Secreting Cells, Young Adult
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