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Serum cortisol/cortisone ratio after Synacthen stimulation.
M Vogeser1, R Zachoval, K Jacob
1Institute of Clinical Chemistry, Ludwig-Maximilians-Universität Munich, Klinikum Grosshadern, 81366, Munich, Germany. mvogeser@klch.med.uni-muenchen.de
Clinical Biochemistry
|August 28, 2001
Summary
Adrenocorticotropic hormone (ACTH) stimulates 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) activity, increasing active cortisol levels by converting inactive cortisone. This study shows ACTH influences peripheral cortisol metabolism.
Area of Science:
- Endocrinology
- Metabolic research
Background:
- 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes regulate cortisol activity.
- 11beta-HSD type 1 in the liver may restore active cortisol from inactive cortisone.
- This mechanism could be crucial during stressful situations.
Purpose of the Study:
- To investigate the influence of exogenous ACTH on the serum cortisol/cortisone ratio.
- To test the hypothesis that ACTH stimulates systemic 11beta-HSD type 1 activity.
Main Methods:
- Prospective collection of paired serum samples from 40 patients before and 1 hour after ACTH stimulation.
- Measurement of serum cortisol and cortisone using LC-ESI/MS/MS.
- Analysis of the cortisol/cortisone ratio.
Main Results:
- Serum cortisol increased by 109% after ACTH administration.
- Serum cortisone significantly decreased by 31% (p < 0.001).
- The cortisol/cortisone ratio increased significantly in all subjects.
Conclusions:
- Exogenous ACTH modulates peripheral cortisol metabolism.
- ACTH stimulates systemic 11beta-HSD type 1 activity.
- This leads to the conversion of inactive cortisone to active cortisol.