β-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome
Open accessAbstract
Glucocorticoids (GCs) are stress hormones primarily responsible for mobilizing glucose to the circulation. Due to this effect, insulin resistance and glucose intolerance are concerns in patients with endogenous overproduction of GCs and in patients prescribed GC-based therapy. In addition, hypercortisolemic conditions share many characteristics with the metabolic syndrome. This study reports on a thorough characterization, in terms of glucose control and lipid handling, of a mouse model where corticosterone is given via the drinking water. C57BL/6J mice were treated with corticosterone (100 or 25 μg/ml) or vehicle in their drinking water for 5 weeks after which they were subjected to insulin or glucose tolerance tests. GC-treated mice displayed increased food intake, body weight gain, and central fat deposit accumulations. In addition, the GC treatment led to dyslipidemia as well as accumulation of ectopic fat in the liver and skeletal muscle, having a substantial negative effect on insulin sensitivity. Also glucose intolerance and hypertension, both part of the metabolic syndrome, were evident in the GC-treated mice. However, the observed effects of corticosterone were reversed after drug removal. Furthermore, this study reveals insights into β-cell adaptation to the GC-induced insulin resistance. Increased pancreatic islet volume due to cell proliferation, increased insulin secretion capacity, and increased islet chaperone expression were found in GC-treated animals. This model mimics the human metabolic syndrome. It could be a valuable model for studying the complex mechanisms behind the development of the metabolic syndrome and type 2 diabetes, as well as the multifaceted relations between GC excess and disease.
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Chronic administration of corticosterone in drinking water leads to hyperglycaemia, insulin resistance and dyslipidaemia in rodents.
“Chronic administration of corticosterone in drinking water leads to hyperglycaemia, insulin resistance and dyslipidaemia in rodents 10, 11.”
From Type 2 diabetes mellitus and psychological stress — a modifiable risk factor (2017) · cites this paper as [11]
The dyslipidemia and glucose-control Results sections report dyslipidemia and insulin resistance in mice given corticosterone in drinking water. They report postprandial hyperglycaemia only at the higher dose; mice given the lower dose remained euglycaemic, and fasting glucose did not increase at either dose. The unqualified hyperglycaemia claim therefore overstates the finding. (LLM, conf=0.88)
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Systems Pharmacology: Enabling Multidimensional Therapeutics
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- Authors
- Fransson, L., Franzén, S., Rosengren, V., Wolbert, P., Sjöholm, Å., & Ortsäter, H.
- Affiliations
- Linköping University (SE)
- University of South Alabama (US)
- Karolinska Institutet (SE)
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2013-09-17
- Volume
- 219
- Issue
- 3
- Pages
- 231-241
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2110172023
- Cited by
- 59
- References
- 55
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 8 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 8 · 2015: 1 · 2014: 3 · 2013: 1
- FWCI
- 4.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Tore Nilsons Stiftelse för Medicinsk Forskning
- Diabetes Research and Wellness Foundation
- Svenska Sällskapet för Medicinsk Forskning
- Karolinska Institutet
- Diabetesfonden
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- glucocorticoids, corticosterone, metabolic syndrome, beta-cell adaptation, insulin resistance, impaired glucose tolerance, hypercortisolism, dyslipidemia, ectopic fat deposition, insulin secretion, hypertension, type 2 diabetes, mouse model
- MeSH terms
- Administration, Oral, Animals, Behavior, Animal, Energy Intake, Disease Models, Animal, Glucocorticoids, Insulin Resistance, Liver, Male, Mice, Inbred C57BL, Stress, Physiological, Stress, Psychological, Weight Gain, Muscle, Skeletal, Metabolic Syndrome, Adiposity, Dyslipidemias, Insulin-Secreting Cells, Mice, Allostasis
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