GH effect on enzyme activity of 11betaHSD in abdominal obesity is dependent on treatment duration

• Published in: European journal of endocrinology Vol. 154; no. 1; pp. 69 - 74
• Main Authors: Sigurjónsdóttir, Helga A, Koranyi, Josef, Axelson, Magnus, Bengtsson, Bengt-Ake, Johannsson, Gudmundur
• Format: Journal Article
• Language: English
• Published: England 01.01.2006
• Subjects: 11-beta-Hydroxysteroid Dehydrogenase Type 1; 11-beta-Hydroxysteroid Dehydrogenase Type 1 - blood; 11-beta-Hydroxysteroid Dehydrogenase Type 2; 11-beta-Hydroxysteroid Dehydrogenase Type 2 - blood; 11-beta-Hydroxysteroid Dehydrogenases; 11-beta-Hydroxysteroid Dehydrogenases - blood; 11-beta-Hydroxysteroid Dehydrogenases - drug effects; Abdominal Fat; Abdominal Fat - drug effects; administration & dosage; blood; drug effects; drug therapy; enzymology; Human Growth Hormone; Human Growth Hormone - administration & dosage; Human Growth Hormone - therapeutic use; Humans; Hydrocortisone; Hydrocortisone - blood; Insulin Resistance; Insulin Resistance - physiology; Male; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; Middle Aged; Obesity; Obesity - drug therapy; Obesity - enzymology; physiology; therapeutic use; Time Factors
• ISSN: 0804-4643
• DOI: 10.1530/eje.1.02061

In the past years the interaction of GH and 11beta hydroxysteroid dehydrogenase (11betaHSD) in the pathogenesis of central obesity has been suggested. We studied the effects of 9 months of GH treatment on 11betaHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 48-66 years, in a randomised, double-blind, placebo-controlled trial. Urinary steroid profile was used to estimate 11betaHSD type 1 and 2 (11betaHSD1 and 11betaHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemic-hyperinsulinaemic glucose clamp was used to assess insulin sensitivity. In the GH-treated group the 11betaHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11betaHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11betaHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11betaHSD1 and 11betaHSD 2 and changes in GDR. The study demonstrates that short- and long-term GH treatment has different effects on 11betaHSD1 and 11betaHSD2 activity. Moreover, the data do not support that long-term metabolic effects of GH are mediated through its action on 11betaHSD.