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Response of the Pituitary-Adrenal Axis to Hypoglycemic Stress in Women with the Polycystic Ovary Syndrome

Departments of Obstetrics and Gynecology (G.G., J.H., U.L., T.B.), Clinical Chemistry (M.S.), and Internal Medicine (C.B.), Akademiska Hospital, Uppsala University, S-751 85 Uppsala, Sweden; and the Department of Obstetrics and Gynecology, S. Anna Hospital, Torino University (M.M.), 10126 Torino, Italy

Address all correspondence and requests for reprints to: Dr. Gianluca Gennarelli, Department of Obstetrics and Gynecology, Akademiska Hospital, Uppsala University, S-751 85 Uppsala, Sweden.

The role of the adrenals in the polycystic ovary syndrome (PCOS) is debated. Both single steroid-converting enzyme abnormalities and increased adrenal activity have received support. The conventional Synacthen test using pharmacological doses of ACTH results in unphysiological levels of ACTH. Therefore, we used insulin-induced hypoglycemia (0.15 IU/kg BW) to asses the responses of ACTH, cortisol, pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and androstenedione in 18 women with PCOS and in 17 normal women of similar age and body mass index. The blood glucose concentration at 30 min was 2 mmol/L or less in all women, i.e. well below the threshold of the hormonal counterregulatory response. The women with PCOS showed a lower ACTH response, expressed as the maximum increment above basal [mean (95% confidence interval): PCOS, 11.1 (6.9–15.3); controls, 19.9 (13.8–26) pmol/L; P < 0.05], but a quantita-tively comparable [PCOS, 207.2 (148.5–266.5); controls, 167.1 (100.6–233.2) nmol/L; P = NS] and more prompt cortisol response than the controls (by ² test, P < 0.05), resulting in a higher molar ratio between the maximum increments of cortisol and ACTH [PCOS, 13.9 (8.7–19); controls, 8.8 (5.7–12); P < 0.05]. The women with PCOS did, however, show a more rapid decline in cortisol levels than the controls (P < 0.05 at 120 and 180 min). The responses of the androgens and intermediate adrenal steroids were similar in women with PCOS and controls. The findings suggest an adaptation to increased adrenal reactivity to endogenous ACTH in women with PCOS. Exposure to hypoglycemia as a model of stress was not followed by hypersecretion of adrenal androgens and revealed no signs of steroid enzyme disturbances in women with PCOS.

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