SFEBES2022 Oral Communications Adrenal and Cardiovascular (6 abstracts)
Glucocorticoid excess elevates metabolic rate via a 11β-HSD1 dependent mechanism in C57BL/6J mice
Samuel Heaselgrave 1 , Silke Heising 1 , Stuart Morgan 2 , Ali Kabli 1 , Michael Sagmeister 1 , Rowan Hardy 1 , Craig Doig 2 , Nicholas Morton 3 , Kostas Tsintzas 4 & Gareth Lavery 2
1University of Birmingham, Birmingham, United Kingdom; 2Nottingham Trent University, Nottingham, United Kingdom; 3University of Edinburgh, Edinburgh, United Kingdom; 4University of Nottingham, Nottingham, United Kingdom
Introduction: Glucocorticoids are vital metabolic regulators. However, glucocorticoid excess (GE) causes severe metabolic dysfunction, ultimately leading to Cushing’s Syndrome. This dysfunction is often dependent on the presence of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Whether GE also alters metabolic rate, and whether this is also dependent on 11β-HSD1, remains unclear.
Methods: Male and female wild-type (WT) C57BL/6J and 11β-HSD1KO mice were treated with corticosterone or vehicle control ad libitum via drinking water for 3 weeks. Mice were housed in a TSE Phenomaster for the final week of treatment for comprehensive metabolic assessment.
Results: Corticosterone treatment in WT mice resulted in a phenotype typical of GE, however female mice experienced greater fat accumulation. 11β-HSD1KO mice did not experience this phenotype. Corticosterone treatment elevated energy expenditure (EE) in female WT mice during the day alone (25±5.9%). Male WT mice did not experience a significant increase. Corticosterone did significantly elevate the respiratory exchange ratio (RER) towards 1 in both male (10.7±5.7%) and female (11.8±7.0%) WT mice during the day. RER remained elevated in female WT mice (7.6±4.8%) and moderately so in male WT mice (3.2±2.6%) at night. Activity, assessed in female WT mice only, was continually decreased by corticosterone treatment (-53.1±54.8%). Corticosterone treated WT mice became hyperphagic and polydipsic, continuously consuming more than controls. Male or female 11β-HSD1KO mice treated with corticosterone did not experience these effects.
Conclusion: These findings provide further insights into the metabolic consequences of GE as well as the dependency on 11β-HSD1 to facilitate them. Whilst elevations are seen in both male and female WT mice, they are greater in females. Activity is decreased meaning it is not responsible for the elevations. However, hyperphagia and the subsequent chemical energy cost of de novo lipogenesis might be responsible and merits further investigation.
Volume 86
Article tools
My recent searches
My recently viewed abstracts
Authors
Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
© Bioscientifica 2024 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more