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Samuel R Heaselgrave Center of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, Nottingham Trent University, Birmingham, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Silke Heising Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Stuart A Morgan Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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David M Carthwright Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Michael Sagmeister Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Rowan S Hardy Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Craig L Doig Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, Nottingham Trent University, Birmingham, UK

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Nicholas Morton Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, Nottingham Trent University, Birmingham, UK
Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK

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Kostas Tsintzas MRC Versus Arthritis Centre for Musculoskeletal Ageing Research, School of Life Sciences, University of Nottingham, Queen’s Medical Centre, Nottingham, UK

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Gareth G Lavery Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, Nottingham Trent University, Birmingham, UK

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Systemic glucocorticoid excess causes several adverse metabolic conditions, most notably Cushing’s syndrome. These effects are amplified by the intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Here, we determined the less well-characterised effects of glucocorticoid excess, and the contribution of 11β-HSD1 amplification on metabolic rate in mice. Male and female C57BL/6J (wild type, WT) and 11β-HSD1 knockout (11β-HSD1 KO) mice were treated with high-dose corticosterone or a vehicle control for 3 weeks. Indirect calorimetry was conducted during the final week of treatment, with or without fasting, to determine the impact on metabolic rate. We found that corticosterone treatment elevated metabolic rate and promoted carbohydrate utilisation primarily in female WT mice, with effects more pronounced during the light phase. Corticosterone treatment also resulted in greater fat accumulation in female WT mice. Corticosterone induced hyperphagia was identified as a likely causal factor altering the respiratory exchange ratio (RER) but not energy expenditure (EE). Male and female 11β-HSD1 KO mice were protected against these effects. We identify novel metabolic consequences of sustained glucocorticoid excess, identify a key mechanism of hyperphagia, and demonstrate that 11β-HSD1 is required to manifest the full metabolic derangement.

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