GLP-1 Receptor Agonist Therapy for Glucocorticoid-Induced Dysglycaemia: A Systematic Review.

Authors

Aleksandra Jędrasek, Wiktoria Ulicka, Karolina Lisowska, Anna Fabiańska, Jolanta Małyszko, Leszek Czupryniak

Published in

Diabetes, obesity & metabolism. Oct 08, 2026. Epub Oct 08, 2026.

Abstract

Glucocorticoids (GCs) commonly induce glycaemic disturbance, from transient steroid-induced hyperglycaemia to steroid-induced diabetes and contribute to post-transplant diabetes mellitus (PTDM). Insulin remains the standard treatment for GC-induced glycaemic dysregulation. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have a mechanistic rationale here, but their efficacy and safety in GC-induced dysglycaemia have not been systematically appraised.
A systematic review was conducted in accordance with PRISMA 2020 guidelines (registration number: CRD420251183082). Embase, PubMed/MEDLINE and the Cochrane Library were searched up to May 2026. A structured narrative synthesis was the primary method.
Thirteen studies were included, predominantly retrospective cohort studies; 10 enrolled solid organ transplant recipients with PTDM or pre-existing type 2 diabetes. GLP-1 RA therapy, either as monotherapy or as an adjunct to insulin, was associated with reductions in HbA1c and body weight, and a low rate of hypoglycaemia in the majority of included studies. GLP-1 RAs led to insulin dose reduction or discontinuation, reducing injection frequency and treatment burden. Five studies contributed to at least one pooled estimate, and no outcome was informed by more than three studies; given substantial heterogeneity and very low GRADE certainty, these estimates are exploratory and are presented in Supplementary Material 2.
Individual studies reported reductions in HbA1c, body weight and insulin dose, with a low rate of hypoglycaemia episodes. However, available data specific to GC-induced dysglycaemia remain insufficient. Prospective controlled trials with explicit characterisation of GC exposure are required.

PMID:
42850058
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

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