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Clinical investigation of 11 beta-hydroxysteroid dehydrogenase
1University of Edinburgh, Department of Medicine, Western General Hospital, Scotland, UK.
Abstract:
At least two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) have been identified, and clinical studies have illustrated their physiological and pathological significance. In the kidney, a high affinity 11 beta-OHSD2 inactivates cortisol to cortisone and protects mineralocorticoid receptors from cortisol. In the liver, a low affinity 11 beta-OHSD1 converts cortisone to cortisol, and may ensure that glucocorticoid receptors are adequately exposed to cortisol. In vascular smooth muscle, the conversion of cortisol to cortisone influences vascular tone. Defects in 11 beta-OHSD2 probably account for mineralocorticoid excess in the syndromes of Apparent Mineralocorticoid Excess, licorice administration, and ectopic ACTH syndrome. Defects in 11 beta-OHSD1 may be important in essential hypertension, and polycystic ovarian syndrome. The underlying mechanism for all of these defects, and the putative role of endogenous inhibitors of 11 beta-OHSD, remains unclear. In future, the measurement of the activity of individual isoforms should resolve this uncertainty.
Insights
Two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) play distinct roles in hormone regulation. Understanding their defects is crucial for treating conditions like hypertension and Cushing
Area of Science:
- Endocrinology
- Molecular Biology
- Physiology
Background:
- Two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) exist with distinct tissue-specific functions.
- 11 beta-OHSD2 in the kidney inactivates cortisol, while 11 beta-OHSD1 in the liver activates cortisone.
Purpose of the Study:
- To elucidate the physiological and pathological significance of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) isoforms.
- To explore the role of 11 beta-OHSD defects in various endocrine and metabolic disorders.
Main Methods:
- This study is a review of existing clinical and physiological data.
- Analysis of the known functions and implications of 11 beta-OHSD1 and 11 beta-OHSD2 isoforms.
Main Results:
- 11 beta-OHSD2 defects are linked to apparent mineralocorticoid excess syndromes.
- 11 beta-OHSD1 defects may contribute to essential hypertension and polycystic ovarian syndrome.
Conclusions:
- The precise mechanisms underlying 11 beta-OHSD defects and the role of endogenous inhibitors require further investigation.
- Measuring individual 11 beta-OHSD isoform activity is proposed to resolve current uncertainties.