Insulin-resistance is a well-known feature of polycystic ovary syndrome (PCOS) and the present paper investigates the comparative roles of the peripheral tissues and the pancreatic beta-cells in its pathogenesis. The study was conducted on 5 young women with PCOS, all of normal weight and glucose tolerance in whom the glucose-insulin clamp test had revealed reduced peripheral glucose uptake that was not influenced by other conditions typically associated with insulin-resistance. Beta-cell function was investigated in these patients and 5 healthy controls via the assessment of the efficiency of the insulin/insulin feedback which involved studying the suppression of plasma C peptide during the glucose clamp. The results suggested that the insulin/insulin beta-cell feedback mechanism had retained its efficiency despite proven peripheral insulin-resistance. These data do not therefore support the hypothesis advanced by others that there is some sort of beta-cell insulin resistance parallel to the insulin resistance of the peripheral tissues. On the basis of those results it is rather believed that in PCOS the insulin-resistance is generated peripherally while the insulin/insulin feedback in the beta-cell is unimpaired. This obliges us to rethink the role of the hyperinsulinism encountered in PCOS and suggests that the changed sensitivity of the peripheral tissues to insulin activity may constitute a primary event in the genesis of insulin-resistance. This type of behavior has been demonstrated in the obese and in people with acanthosis nigricans, all with normal glucose tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)