OBJECTIVE Although insulin has been shown to stimulate ovarian steroidogenesis and hyperinsulinaemia has been implicated in the raised androgen levels found in diseases associated with significant insulin resistance, ovarian function has not been studied so far in women with NIDDM. We have assessed ovarian function in women with NIDDM at the early (hyperinsulinaemic) and late (relative insulinopaenic) stages of evolution of the disease after strong stimulation with buserelin, a long‐acting GnRH analogue. Significant differences in ovarian function would be expected, depending on the stage of evolution of NIDDM.DESIGN Following an overnight fast, a standard OGTT (75 g, orally) was performed (0830 h) in all diabetic and control women. Blood samples were obtained for blood glucose, insulin and C‐peptide measurements before and at 30‐minute intervals for 2 hours. On the termination of the OGTT, a buserelin test (100 μg, s.c.) was performed (1030 h) and blood samples were obtained for FSH, LH, Δ4‐androstenedione, total testosterone, free testosterone and oestradiol measurements before and then at 4‐hour intervals for 20 hours.SUBJECTS Thirty‐one women with NIDDM (13 hyperinsulinaemic and 18 with relative insulinopaenia), 12 obese and 11 normally menstruating non‐obese, non‐diabetic women, aged 29–39 years, were studied.RESULTS The integrated response (AUC) of oestradiol to buserelin was found to be normal in hyperinsulinaemic NIDDM and obese non‐diabetic women in the face of an increased free testosterone response, while in relatively insulinopaenic NIDDM women the oestradiol response was significantly reduced in the face of a normal free testosterone response.CONCLUSIONS The results suggest that in women with NIDDM the ovaries have a reduced ability to convert androgen to oestrogen, probably due to a reduction of ovarian aromatase activity. As oestrogens protect against atherogenesis, it is speculated that the relative inability of the ovaries to produce oestradiol in NIDDM women with relative insulinopaenia might be involved in the development of the macroangiopath