Abstract
The commonest side-effects of GH replacement therapy relate to sodium retention but its mechanism is unclear. In rats, GH inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) activities. In man, this action might impair inactivation of cortisol to cortisone in the distal nephron thereby allowing cortisol to activate mineralocorticoid receptors. In this study, we examined the effects of GH replacement on cortisol metabolism.
Original language | English |
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Pages (from-to) | 257-63 |
Number of pages | 7 |
Journal | Clinical Endocrinology |
Volume | 49 |
Issue number | 2 |
Publication status | Published - 1998 |