INFLUENCE OF RESIDUAL INSULIN-SECRETION AND DURATION OF DIABETES-MELLITUS ON THE CONTROL OF LUTEINIZING-HORMONE SECRETION IN WOMEN

Background The aim of the present study was to establish whether the p ersistence of residual beta-cell activity after long-term diabetes mel litus (DM) exerts a protective role on luteinizing hormone (LII) secre tion. Methods The LH responses to stimulation with gonadotropin-releas ing hormone (Gn-RH) (100 mu g in an i.v. bolus) or naloxone (4 mg inje cted in an i.v. bolus, followed by the constant infusion of 8 mg in 2 h) were measured in C-peptide-positive (CpP) and C-peptide-negative (C pN) normally menstruating women with short-term (group 1 < 3 years, Cp P n = 11, CpN n = 11) Or. long-term (group 2 > 10 years, CpP n = II, C pN n = 11) DM and in age-matched normal control subjects (n = 11). Res ults Gn-RH induced significant increments in LH secretion in all group s. Significant LH responses to naloxone were observed in all groups, e xcept in group 2 CpN patients. However, the LH response so either Gn-R H or naloxone was significantly lower in group 1 CpN, group 2 CpP and group 2 CpN patients than in the normal control subjects. Furthermore, the LH response was significantly lower in group 2 CpP than in group 1 CpP patients and in group 2 CpN than in group 1 CpN subjects. Conclu sions These results indicate a role for both deficiency in residual en dogenous insulin secretion and duration of diabetes in the derangement of LH secretory control. The data suggest that the protective role ex erted by residual beta-cell activity on LH secretion during the early years of DM diminishes with time elapsed after the onset of diabetes m ellitus.