Glintborg Dorte, Støving René Klinkby, Hagen Claus, Hermann Anne Pernille, Frystyk Jan, Veldhuis Johannes D, Flyvbjerg Allan, Andersen Marianne
Department of Endocrinology and Metabolism, Odense University Hospital, Denmark.
J Clin Endocrinol Metab. 2005 Oct;90(10):5605-12. doi: 10.1210/jc.2005-0615. Epub 2005 Aug 2.
Low 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 cogonadotropin, and GH disturbances may be an additional pathogenic factor in PCOS. Decreased abdominal fat mass and improved insulin sensitivity during pioglitazone treatment may affect GH secretion.
The objective of the study was to investigate the effect of pioglitazone on GH levels in PCOS.
Thirty insulin-resistant PCOS patients were randomized to either 16 wk pioglitazone (30 mg/d) or placebo treatment. Before and after intervention, levels of fasting insulin, GH, total IGF-I, free IGF-I, IGF binding protein-1, IGF-II, free fatty acids, testosterone, and SHBG were measured. Patients underwent whole-body dual x-ray absorptiometry scans, pyridostigmine-GHRH tests, and 24-h 20-min integrated blood sampling for measurement of GH.
Peak GH and area under the curve for GH in pyridostigmine-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 IGF binding protein-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 levels. No significant changes were observed in Ferriman Gallwey score or androgen levels.
Pioglitazone treatment significantly increased GHRH-stimulated GH levels and 24-h pulsatile GH secretion, probably directly or indirectly due to improved insulin sensitivity.
多囊卵巢综合征（PCOS）患者中普遍存在生长激素（GH）水平低下的情况，这可能与胰岛素抵抗及腹部脂肪量增加有关。GH是一种重要的卵巢促性腺激素，GH紊乱可能是PCOS的另一致病因素。吡格列酮治疗期间腹部脂肪量减少及胰岛素敏感性改善可能会影响GH分泌。
本研究旨在探讨吡格列酮对PCOS患者GH水平的影响。
30例胰岛素抵抗的PCOS患者被随机分为两组，分别接受16周的吡格列酮（30mg/d）治疗或安慰剂治疗。干预前后，测量空腹胰岛素、GH、总胰岛素样生长因子-I（IGF-I）、游离IGF-I、IGF结合蛋白-1、IGF-II、游离脂肪酸、睾酮和性激素结合球蛋白（SHBG）水平。患者接受全身双能X线吸收法扫描、新斯的明-生长激素释放激素（GHRH）试验以及24小时20分钟的GH综合血样采集。
吡格列酮治疗后，新斯的明-GHRH试验中GH的峰值和曲线下面积、24小时平均GH浓度及GH脉冲分泌均显著增加。GH脉冲频率、脉冲持续时间、近似熵水平或基础GH释放无显著变化。IGF结合蛋白-1水平显著升高，而总IGF-I和游离IGF-I无显著差异。吡格列酮治疗显著降低空腹胰岛素和稳态模型评估水平。Ferriman Gallwey评分或雄激素水平无显著变化。
吡格列酮治疗显著增加了GHRH刺激的GH水平和24小时的GH脉冲分泌，这可能直接或间接归因于胰岛素敏感性的改善。
