SERUM ANDROGEN CHANGES DURING MEAL-INDUCED HYPERINSULINEMIA AND AFTERACUTE SEQUENTIAL BLOCKADE AND HYPERSTIMULATION OF INSULIN RELEASE IN WOMEN WITH POLYCYSTIC-OVARY-SYNDROME

Citation
A. Parra et al., SERUM ANDROGEN CHANGES DURING MEAL-INDUCED HYPERINSULINEMIA AND AFTERACUTE SEQUENTIAL BLOCKADE AND HYPERSTIMULATION OF INSULIN RELEASE IN WOMEN WITH POLYCYSTIC-OVARY-SYNDROME, Archives of medical research, 26, 1995, pp. 209-217
Citations number
30
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
01884409
Volume
26
Year of publication
1995
Pages
209 - 217
Database
ISI
SICI code
0188-4409(1995)26:<209:SACDMH>2.0.ZU;2-5
Abstract
To investigate if acute changes in endogenous insulin release are asso ciated with similar changes in serum androgen, 13 healthy ovulatory wo men (group 1) and six women with polycystic ovary syndrome (PCOS) and hyperinsulinemia, three with acanthosis nigricans (group 2) were studi ed. On day 1 all women ingested a 725 kilocalories breakfast between 7 :30 and 8:00 A.M. The next day (day 2) only PCOS women had the breakfa st and a simultaneous 90-min intravenous infusion of epinephrine (E, 6 mu g/ min) and propranolol (P, 80 mu g/min). On both days serum gluco se, insulin, cortisol, 17 alpha hydroxyprogesterone (17 OI-IP), dehydr oepiandrosterone sulfate (DHEAS), free testosterone (free T), and andr ostenedione (A) were determined every 30 min for a period of 3 h. In g roup 1, glucose, insulin, free T, and DHEAS simultaneously rose (p les s than or equal to 0.026) while cortisol and 17 OHP fell (p less than or equal to 0.020). Group 2 on day 1 had fasting and meal-stimulated h yperinsulinemia but all serum steroids progressively decreased. In onl y one woman free T rose. On day 2 during the E + P infusion, glucose i ncreased yet fasting insulin remained constant and serum steroids decr eased again. During the 90 min post-infusion, insulin sharply increase d but no acute elevation in any steroid occurred. In conclusion, in PC OS women no parallel changes in serum androgen concentrations were see n in association with acute truly physiologic endogenous hyperinsuline mia or during the acute pharmacologically induced hypoinsulinemia and subsequent hyperinsulinemia.