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This version published online on August 2, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-0615
A more recent version of this article appeared on October 1, 2005
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Submitted on March 21, 2005
Accepted on July 25, 2005

Pioglitazone treatment increases spontaneous growth hormone secretion and stimulated growth hormone levels in polycystic ovary syndrome

Dorte Glintborg MD*, René Klinkby Støving MD, PhD, Claus Hagen MD, MSc, Anne Pernille Hermann MD, PhD, Jan Frystyk MD, MSc, Johannes D. Veldhuis MD, Allan Flyvbjerg MD, MSc, and Marianne Andersen MD, PhD

Department of Endocrinology and Metabolism, Odense University Hospital, DK-5000 Odense C, Denmark, Medical Research Laboratories, Clinical Institute, and Medical Department M (Diabetes and Endocrinology), Aarhus University Hospital, DK-8000 Aarhus, Denmark, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Clinical Research Center, Rochester, USA; Department of Endocrinology and Metabolism, Odense University Hospital, DK-5000 Odense C, Denmark; Medical Research Laboratories, Clinical Institute, and Medical Department M (Diabetes and Endocrinology), Aarhus University Hospital, DK-8000 Aarhus, Denmark; Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Clinical Research Center, Rochester, USA

* To whom correspondence should be addressed. E-mail: dorte.glintborg{at}dadlnet.dk.

Background: Low growth hormone (GH) levels, probably due to insulin resistance and increased abdominal fat mass, are well described in polycystic ovary syndrome (PCOS). GH acts as an important ovarian co-gonadotropin and GH disturbances may be an additional pathogenic factor in PCOS. Decreased abdominal fat mass and improved insulin sensitivity during pioglitazon treatment may affect GH secretion.

Objective: To investigate the effect of pioglitazone on GH levels in PCOS.

Design: Thirty insulin resistant PCOS patients were randomized to either 16 weeks of pioglitazone (30 mg/day) or placebo treatment. Before and after intervention, levels of fasting insulin, GH, total insulin-like growth factor (IGF)-I, free IGF-I, IGFBP-1, IGF-II, free fatty acids (FFA), testosterone, and sex hormone binding globulin (SHBG) were measured. Patients underwent whole body dual x-ray absorptiometry (DXA) scans, pyridostigmine (PD)-GH-releasing-hormone (GHRH) tests, and 24 h 20 min.-integrated blood sampling for measurement of GH.

Results: Peak GH and area under the curve (AUC) for GH in PD-GHRH tests and 24 h mean GH concentrations and pulsatile GH secretion significantly increased after pioglitazone treatment. No significant changes were observed in GH pulse frequency, pulse duration, approximate entropy levels, or basal GH release. Levels of IGFBP-1 significantly increased, whereas no significant differences were measured in total IGF-I and free IGF-I. Pioglitazone treatment significantly decreased fasting insulin and homeostasis model assessment (HOMA-r) levels. No significant changes were observed in Ferriman Gallwey-score or androgen levels.

Conclusion: Pioglitazone treatment significantly increased GHRH-stimulated GH levels and 24 h pulsatile GH secretion probably directly or indirectly due to improved insulin sensitivity.
Key words: PCOS • PPARgamma • Pioglitazone • growth hormone • IGF-I • insulin resistance




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