To investigate the effect of a chronic anti-opioid treatment on the adrenal steroid production in polycystic ovarian syndrome (PCOS), 20 women affected by PCOS were studied before and after 6 weeks of treatment with an opioid antagonist. All women had an oral glucose tolerance test (OGTT) (75 g) on day 5 of the cycle. At 11.00 p.m. 2 mg of dexamethasone was orally administered and blood samples collected the following day at 7.00 a.m. Then 250 μgof adrenocortkotrophin hormone (ACTH) was injected i.v. and samples collected 60 min later. At this time a 6 week course of naltrexone treatment (50 mg/day orally) was started, following which the protocol was repeated on day 6-7 of the menstrual cycle. According to OGTT responses, 10 patients were classified as hyperinsulinaemic and 10 as normoinsulin-aemic. No difference in baseline hormone concentrations was found, except for sex hormone-binding globulin, which was significantly greater in normoinsulinaemic patients (P < 0.02). The plasma concentration of all steroids after dexamethasone and ACTH administration was similar in both groups, except for androstenedione (P < 0.02) and 17α-hydroxyprogesterone (17-OHP) (P < 0.05), which were significantly greater after ACTH injection in hyperinsulinaemic compared with normoinsulinaemic PCOS patients. Naltrexone treatment significantly (P < 0.001) reduced insulin response to OGTT in the hyperinsulinaemic group, while it did not affect the response in the normoinsulinaemic group; thus at the end of the treatment the two groups had the same insulin concentrations. Similarly, naltrexone abolished the difference between normoinsulinaemic and hyperinsulinaemic patients regarding androstenedione and 17-OHP response to ACTH. These data confirm that insulin may in part affect the responsiveness of the adrenal glands to ACTH, so that modifications of its plasma concentrations can in turn modify adrenal steroid production. © 1994 Oxford University Press.
Endocrinology: Differential androgen response to adrenocorticotrophin hormone stimulation and effect of opioid antagonist on insulin secretion in polycystic ovarian syndrome
Guido M.;
1994-01-01
Abstract
To investigate the effect of a chronic anti-opioid treatment on the adrenal steroid production in polycystic ovarian syndrome (PCOS), 20 women affected by PCOS were studied before and after 6 weeks of treatment with an opioid antagonist. All women had an oral glucose tolerance test (OGTT) (75 g) on day 5 of the cycle. At 11.00 p.m. 2 mg of dexamethasone was orally administered and blood samples collected the following day at 7.00 a.m. Then 250 μgof adrenocortkotrophin hormone (ACTH) was injected i.v. and samples collected 60 min later. At this time a 6 week course of naltrexone treatment (50 mg/day orally) was started, following which the protocol was repeated on day 6-7 of the menstrual cycle. According to OGTT responses, 10 patients were classified as hyperinsulinaemic and 10 as normoinsulin-aemic. No difference in baseline hormone concentrations was found, except for sex hormone-binding globulin, which was significantly greater in normoinsulinaemic patients (P < 0.02). The plasma concentration of all steroids after dexamethasone and ACTH administration was similar in both groups, except for androstenedione (P < 0.02) and 17α-hydroxyprogesterone (17-OHP) (P < 0.05), which were significantly greater after ACTH injection in hyperinsulinaemic compared with normoinsulinaemic PCOS patients. Naltrexone treatment significantly (P < 0.001) reduced insulin response to OGTT in the hyperinsulinaemic group, while it did not affect the response in the normoinsulinaemic group; thus at the end of the treatment the two groups had the same insulin concentrations. Similarly, naltrexone abolished the difference between normoinsulinaemic and hyperinsulinaemic patients regarding androstenedione and 17-OHP response to ACTH. These data confirm that insulin may in part affect the responsiveness of the adrenal glands to ACTH, so that modifications of its plasma concentrations can in turn modify adrenal steroid production. © 1994 Oxford University Press.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
