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CLINICAL STUDY |
Research Centre for Endocrinology and Metabolism, Sahlgrenska University Hospital, 41345 Gothenburg, Sweden and 1 Department of Clinical Chemistry, Karolinska Hospital, Stockholm, Sweden
(Correspondence should be addressed to H Á Sigurjónsdóttir; Email: helga.sigurjonsdottir{at}medic.gu.se)
Objective: In the past years the interaction of GH and 11ßhydroxysteroid dehydrogenase (11ßHSD) in the pathogenesis of central obesity has been suggested.
Design: We studied the effects of 9 months of GH treatment on 11ßHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 4866 years, in a randomised, double-blind, placebo-controlled trial.
Methods: Urinary steroid profile was used to estimate 11ßHSD type 1 and 2 (11ßHSD1 and 11ßHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemichyperinsulinaemic glucose clamp was used to assess insulin sensitivity.
Results: In the GH-treated group the 11ßHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11ßHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11ßHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11ßHSD1 and 11ßHSD 2 and changes in GDR.
Discussion: The study demonstrates that short- and long-term GH treatment has different effects on 11ßHSD1 and 11ßHSD2 activity. Moreover, the data do not support that long-term metabolic effects of GH are mediated through its action on 11ßHSD.
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