DYSFUNCTION OF THE GROWTH-HORMONE INSULIN-LIKE GROWTH-FACTOR-I AXIS IN WOMEN WITH POLYCYSTIC OVARIAN SYNDROME

OBJECTIVE Although a defect in GH regulation has been suggested in women with polycystic ovarian syndrome (PCOS), the data are limited and mechanism obscure. We have assessed the function of the GH/IGF-I axis in women with PCOS by measuring basal IGF-I levels and the ability of the pituitary to secrete GH following dopamine and GHRH. DESIGN For each woman the complete study lasted 3 days. On the 1st and 2nd days, saline (0.9%, 5 ml/h for 3 h) and dopamine (4 mu g/kg/min for 3 h) infusion tests were performed, respectively, in all FOGS and control women. Blood samples for GH measurement were obtained before and at 20-minute intervals for 3 hours. On the 3rd day a GHRH test (100 mu g, i.v.bolus) was performed in 9 of the women with PCOS and in 9 controls. Blood samples for GH measurements were obtained before and at all-minute intervals for 3 hours. Basal IGF-I levels were measured in the basal blood samples from the saline infusion test in all patients studied. SUBJECTS Thirteen women with PCOS and 11 normally menstruating women (control group), aged 18-35 years, were studied. All women with PCOS had hirsutism and oligomenorrhoea since menarche, elevated serum values of at least one ovarian androgen and the typical ultrasound appearances of PCOS. RESULTS Growth hormone releasing hormone (GHRH) induced a significant increase in GH secretion in both control and PCOS groups. However, the GH response to GHRH was found to be significantly lower in women with PCOS. The 3-hour infusion of dopamine induced a significant increase in GH levels only in the control group, while it failed to stimulate GH release in the women with PCOS. Although both dopamine and GHRH failed to induce a normal GH response in women with PCOS, their IGF-I levels did not differ significantly from those observed in control women. CONCLUSIONS The diminished GH responses to both GHRH and dopamine in women with PCOS, in the presence of normal circulating IGF-I levels, suggests a dysregulation in GH secretion. Although the data are suggestive of a hypothalamic defect, further studies are required to clarify the underlying mechanism and the role, if any, of GH in the pathogenesis of polycyctic ovarian syndrome

The interaction of growth hormone releasing hormone with other hypothalamic hormones on the release of anterior pituitary hormones.

To determine whether the 29 amino-acid fragment of growth hormone releasing hormone (GHRH) can be combined with other hypothalamic releasing hormones in a single test of anterior pituitary reserve, the responses of anterior pituitary hormones to combinations of an i.v. bolus of GHRH(1-29)NH2 or saline with an i.v. bolus of either LH releasing hormone (LHRH) plus TRH, ovine CRH(oCRH) or saline were studied. Each infusion of GHRH(1-29)NH2 resulted in a rapid increment of the plasma GH value. Infusion of GHRH(1-29)NH2 also caused a small and transient rise in plasma PRL, but no change in the integrated PRL response. The combination of GHRH(1-29)NH2 with LHRH plus TRH caused a larger increment of peak and integrated plasma TSH levels than LHRH plus TRH alone. GHRH(1-29)NH2 did not affect the release of other anterior pituitary hormones after infusion with oCRH or LHRH plus TRH. Because of the finding of potentiation of the TSH-releasing activity of LHRH plus TRH by GHRH(1-29)NH2, the study was extended to the investigation of TSH release after infusion of TRH in combination with either GHRH(1-29)NH2 or GHRH(1-40). In this study the combination of TRH with both GHRH preparations also caused a larger increment of the peak and integrated plasma TSH levels than TRH alone. It is concluded that GHRH(1-29)NH2 possesses moderate PRL-releasing activity apart from GH-releasing activity. In addition, GHRH potentiates the TSH-releasing activity of TRH.(ABSTRACT TRUNCATED AT 250 WORDS