The DOI matches its Crossref record; 125 of the 125 references it cites were found in a registry or an index.
Glucocorticoid treatment and endocrine pancreas function: implications for glucose homeostasis, insulin resistance and diabetes
Open accessAbstract
Glucocorticoids (GCs) are broadly prescribed for numerous pathological conditions because of their anti-inflammatory, antiallergic and immunosuppressive effects, among other actions. Nevertheless, GCs can produce undesired diabetogenic side effects through interactions with the regulation of glucose homeostasis. Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. In addition, GCs can promote abdominal obesity, elevate plasma fatty acids and triglycerides, and suppress osteocalcin synthesis in bone tissue. In response to GC-induced peripheral IR and in an attempt to maintain normoglycaemia, pancreatic β-cells undergo several morphofunctional adaptations that result in hyperinsulinaemia. Failure of β-cells to compensate for this situation favours glucose homeostasis disruption, which can result in hyperglycaemia, particularly in susceptible individuals. GC treatment does not only alter pancreatic β-cell function but also affect them by their actions that can lead to hyperglucagonaemia, further contributing to glucose homeostasis imbalance and hyperglycaemia. In addition, the release of other islet hormones, such as somatostatin, amylin and ghrelin, is also affected by GC administration. These undesired GC actions merit further consideration for the design of improved GC therapies without diabetogenic effects. In summary, in this review, we consider the implication of GC treatment on peripheral IR, islet function and glucose homeostasis.
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Metadata
- Authors
- Rafacho, A., Ortsäter, H., Nadal, A., & Quesada, I.
- Affiliations
- Universitat de Miguel Hernández d'Elx (ES)
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2014-09-30
- Volume
- 223
- Issue
- 3
- Pages
- R49-R62
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2170071103
- Cited by
- 216
- References
- 124
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 21 · 2023: 14 · 2022: 19 · 2021: 18 · 2020: 18 · 2019: 27 · 2018: 27 · 2017: 16 · 2016: 22 · 2015: 15 · 2014: 1
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
- Funders
- European Foundation for the Study of Diabetes
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (471397/2011-3)
- Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas
- Instituto de Salud Carlos III
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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
- glucocorticoids, diabetogenic effect, glucose homeostasis, insulin resistance, beta-cell function, hyperinsulinemia, hyperglycemia, hyperglucagonaemia, islet hormones, somatostatin, amylin, ghrelin, osteocalcin, abdominal obesity, insulin signaling
- MeSH terms
- Animals, Blood Glucose, Diabetes Mellitus, Type 2, Glucocorticoids, Glucose, Homeostasis, Humans, Insulin Resistance, Islets of Langerhans, Models, Biological
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