Growth hormone replacement inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenases in ACTH-deficient patients

B R Walker, R Andrew, K M MacLeod, P L Padfield

Research output: Contribution to journalArticlepeer-review

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 languageEnglish
Pages (from-to)257-63
Number of pages7
JournalClinical Endocrinology
Volume49
Issue number2
Publication statusPublished - 1998

Fingerprint

Dive into the research topics of 'Growth hormone replacement inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenases in ACTH-deficient patients'. Together they form a unique fingerprint.

Cite this