The thesis proposes that elevated concentrations of pancreatic glucagon are involved in the development and maintenance of insulin resistance in women with PCO, that there is a positive relationship between the concentrations of glucagon and androgens in women with PCO, and a decrease in the serum concentrations of androgens will reduce the concentration of glucagon in the peripheral plasma. Thus, peripheral insulin resistance will be sustained by counterregulation by increased plasma concentrations of glucagon, but insulin will act unopposed upon the ovary as a somatotrophic or gonadotrophic hormone. To investigate this hypothesis, 24 obese (body mass index, BMI, > 25kgm^-2) and 20 non-obese women with polycystic ovary syndrome (PCO), and 10 obese and 13 non-obese control subjects underwent a 75g oral glucose tolerance test (oGTT). Following alteration of endogenous concentrations of androgens by administration of buserelin, spironolactone or a combination of cyproterone acetate and ethinyl oestradiol to women with PCO, and goserelin or danazol to control subjects, the oGTT was repeated. The change in relationships between glucose, insulin, C-peptide and glucagon values with those of testosterone, androstenedione, dehydroepiandrosterone sulphate and sex hormone binding globulin before and after treatment were examined. Obese women with PCO had higher serum concentrations of insulin and glucose than non-obese women with PCO and control subjects, but plasma concentrations of glucagon were greater in obese control women. There were no relationships between fasting concentrations of insulin or insulin responses to oral glucose in either group of PCO subjects, but the glucagon response to oral glucose was related to both testosterone and androstenedione in obese women with PCO. No relationship was demonstrated between change in serum concentrations of androgens and those of insulin or glucagon in any of the groups.