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Low Amplitude and Disorderly Spontaneous Growth Hormone Release in Obese Women with or without Polycystic Ovary Syndrome

Departments of Endocrinology and Metabolic Diseases (E.W.C.M.v.D., F.R.), General Internal Medicine (A.E.M., H.P.), Clinical Chemistry (M.F.), and Obstetrics, Gynecology and Reproductive Medicine (F.H.H.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands; and Division of Endocrinology, Department of Internal Medicine, General Clinical Research Center, Specialized Cooperative Center for Reproduction Research and Center for Biomathematical Technology, University of Virginia Medical School (J.D.V.), Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Hanno Pijl, M.D., Department of Internal Medicine, Leiden University Medical Center, C1-R39, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail: . h.pijl{at}lumc.nl

Abstract

Obesity is associated with considerably reduced plasma GH concentrations, which may contribute to anovulation in (obese) women with polycystic ovary disease (PCOS). This clinical investigation was undertaken to establish whether the GH release process is deranged in obese women with PCOS and, if so, whether the observed anomalies are features of the syndrome or a sequel of body fat accretion. To this end we sampled 24-h plasma GH concentration profiles at 10-min intervals in 15 obese PCOS patients [mean age, 29 yr (range, 20–38); percent body fat, 47 ± 5.2%], 15 equally obese controls with regular menstrual cycles [age, 34 yr (range, 20–44); percent body fat, 48 ± 4.9%], and 15 healthy age-matched lean controls [age, 34 yr (range, 21–45); percent body fat, 29 ± 9.0%]. Compared with lean controls, obese PCOS patients exhibited a greater than 60% reduction in basal and a greater than 75% reduction in pulsatile and total daily GH secretion due to a 2.7-fold attenuation of burst mass and a lesser (1.4-fold) slowing of GH pulse frequency. The mean ± SEM number of statistically significant GH peaks was 13.9 ± 1.2/24 h, the endogenous GH half-life was 14.1 ± 0.4 min, basal GH secretion was 5.0 ± 0.7 mU/liter·24 h, and total secretion was 61.4 ± 9.6 mU/liter·24 h in obese women with PCOS. None of these parameters differed from those in the body mass index-matched controls. The approximate entropy ratio was significantly increased in obese women (both PCOS and controls), indicating greater irregularity of the GH release process. Total GH secretion in patients and the two control groups correlated strongly and negatively with percent body fat (r = -0.775; P < 10^-8). Serum concentrations of IGF-I and IGF-binding protein-3 were higher in patients with PCOS than in obese controls (P = 0.03 and P = 0.02, respectively), but the IGF-1/IGF-binding protein-3 ratio was equivalent in all three study groups. In conclusion, the profoundly reduced and irregular GH release in obese women with PCOS appears to be a corollary of body fat accretion and not of the syndrome per se.

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