Raised insulin levels are now recognized as a characteristic feature of women with polycystic ovaries (PCO), and hyperinsulinism has been shown to stimulate androgen production in such women. We have, however, recently shown that hyperinsulinaemia is present only in the obese subjects with PCO in whom insulin concentrations correlate with those of luteinizing hormone. We therefore studied 24-hour blood profiles of growth hormone (GH) and insulinlike growth factor-I (IGF-I) in obese and non-obese women with PCO, for comparison with their levels of insulin, C-peptide and other hormones, such as androgens which are known to be disturbed in PCO. Mean 24-hour GH levels were higher overall in PCO than in control subjects, although the difference was not significant. When, however, a separate analysis was made in obese as compared with non-obese PCO patients, GH concentrations were significantly higher in the non-obese group than in the obese (p = 0.0005). There was a significant negative correlation between body mass index and mean 24-hour GH concentrations (r = -0.641; p = 0.0006). IGF-I concentrations were however similar in the PCO group overall and in controls, as well as in the obese and non-obese PCO patients. The 24-hour blood glucose profile pattern was significantly different in PCO women from controls (p = 0.009), with absence of post-prandial peaks in blood glucose concentrations. These changes were most marked in the non-obese PCO group, who also had significantly lower blood glucose levels than either controls or obese PCO subjects. Significantly higher 24-hour C-peptide and insulin concentrations were found in the obese PCO group compared with controls and the non-obese PCO group. The absence of typical post-prandial increases in insulin and C-peptide concentrations was also evident in the non-obese PCO subjects. There was a significant negative correlation between the 24-hour C-peptide and mean 24-hour GH values (r = – 0.629; p = 0.0212) in the PCO group. Our finding of higher GH concentrations in non-obese PCO patients together with lower blood glucose and normal IGF-I concentrations could theoretically be explained in terms of altered IGF-binding protein concentration, which in turn would influence the biological potency of IGF-I and regulation of GH secretion. These findings would also support the concept that part of the disturbance in patients with PCO lies between that of insulin and IGF-I binding protein.