Effects of cortisol on carbohydrate, lipid, and protein metabolism: studies of acute cortisol withdrawal in adrenocortical failure
Abstract
CONTEXT: Cortisol is an important catabolic hormone, but little is known about the metabolic effects of acute cortisol deficiency. OBJECTIVE: The objective of the study was to test whether clinical symptoms of weight loss, fatigue, and hypoglycemia could be explained by altered energy expenditure, protein metabolism, and insulin sensitivity during cortisol withdrawal in adrenocortical failure. DESIGN, PARTICIPANTS, AND INTERVENTION: We studied seven women after 24-h cortisol withdrawal and during replacement control during a 3-h basal period and a 3-h glucose clamp. RESULTS: Cortisol withdrawal generated cortisol levels close to zero, a 10% decrease in basal energy expenditure, increased TSH and T(3) levels, and increased glucose oxidation. Whole-body glucose and phenylalanine turnover were unaltered, but forearm phenylalanine turnover was increased. During the clamp glucose, infusion rates rose by 70%, glucose oxidation rates increased, and endogenous glucose production decreased. Urinary urea excretion decreased by 40% over the 6-h study period. CONCLUSIONS: Cortisol withdrawal increased insulin sensitivity in terms of increased glucose oxidation and decreased endogenous glucose production; this may induce hypoglycemia in adrenocortical failure. Energy expenditure and urea loss decreased, indicating that weight and muscle loss in Addison's disease is caused by other mechanisms, such as decreased appetite. Increased muscle protein breakdown may amplify the loss of muscle protein.
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Cortisol deficiency causes a reduction in endogenous glucose production and an increase in glucose oxidation, which can lead to hypoglycaemia.
“In addition, cortisol deficiency causes a reduction in endogenous glucose production and an increase in glucose oxidation, which can lead to hypoglycaemia (23).”
From Hypoglycaemia in adrenal insufficiency (2023) · cites this paper as [23]
Lack of cortisol has been shown to increase insulin sensitivity, which enhances peripheral tissue's uptake of glucose, thereby increasing the risk of a hypoglycaemia event.
“Lack of cortisol has been shown to increase insulin sensitivity (23), which will enhance peripheral tissue’s uptake of glucose, thereby increasing the risk of a hypoglycaemia event.”
From Hypoglycaemia in adrenal insufficiency (2023) · cites this paper as [23]
Cortisol deficiency increases glucose oxidation and decreases endogenous glucose production.
“Lastly, cortisol deficiency has been found to increase glucose oxidation and decrease endogenous glucose production [34].”
From Non-Diabetic Hypoglycemia: Evaluation and Management in Adults (2025) · cites this paper as [34]
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References 44 · Cited by 176
Research works printed but not linked: 2
- Ten S, New M, Maclaren N 2001 Clinical review 130: Addison's disease 2001. J Clin Endocrinol Metab 86:2909 -2922
- Hangaard J, Andersen M, Grodum E, Koldkjar O, Hagen C 1999 The effects of endogenous opioids and cortisol on thyrotropin and prolactin secretion in patients with Addison's disease. J Clin Endocrinol Metab 84:1595-1601
- Authors
- Christiansen, J. J., Djurhuus, C. B., Gravholt, C. H., Iversen, P., Christiansen, J. S., Schmitz, O., Weeke, J., Jørgensen, J. O. L., & Møller, N.
- Affiliations
- Aarhus University Hospital (DK)
- Medical Department M, Aarhus Sygehus and Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, DK-8000 C Århus, Denmark
- Corresponding author
- Christiansen, Jens Juel
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2007-09-01
- Volume
- 92
- Issue
- 9
- Pages
- 3553-3559
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2089587576
- Cited by
- 176
- References
- 44
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 4 · 2023: 12 · 2022: 13 · 2021: 20 · 2020: 9 · 2019: 17 · 2018: 9 · 2017: 13 · 2016: 11 · 2015: 9 · 2014: 4 · 2013: 11 · 2012: 6
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pfizer
- Novo Nordisk
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- adrenal insufficiency, Addison's disease, energy expenditure, insulin sensitivity, glucose oxidation, endogenous glucose production, protein metabolism, urea excretion, hypoglycemia, weight loss, muscle protein degradation, glucose clamp
- MeSH terms
- Acute Disease, Addison Disease, Adrenal Gland Diseases, Adult, Basal Metabolism, Calorimetry, Indirect, Energy Metabolism, Female, Glucose, Humans, Hydrocortisone, Middle Aged, Proteins, Microdialysis, Withholding Treatment, Carbohydrate Metabolism, Lipid Metabolism
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