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Journal of Clinical Endocrinology & Metabolism, Vol 61, 779-782, Copyright © 1985 by Endocrine Society


ARTICLES

Central opioid activity in polycystic ovary syndrome with and without dopaminergic modulation

RB Barnes and RA Lobo

It has been hypothesized that brain opioid activity may be decreased in patients with the polycystic ovary syndrome (PCO) and that this decrease may, in part, explain the elevated levels of LH characteristic of the syndrome. We, therefore, examined the LH and PRL responses to naloxone infusions (2 mg/h for 4 h) in seven women with PCO and five weight- and estrogen-matched normal women. The infusions were given both before and after pretreatment with L-dopa-carbidopa (L-DOPA-C) because dopaminergic activity may be decreased in PCO, and dopamine may interact with the brain opioid system. Both PCO patients and normal women had similar responses of serum LH during naloxone treatment; the mean maximum LH responses were 53 +/- 15% (+/- SE) in normal women and 51 +/- 12% in PCO patients (P greater than 0.05). PRL levels were also unaffected by naloxone infusion. After L-DOPA-C pretreatment, baseline LH and PRL levels were unchanged in normal women and PCO patients, and the naloxone-induced LH rise was completely abolished in the normal women. However, in PCO patients, LH increased from 24.7 +/- 4 to 31 +/- 5 mIU/ml, with a mean maximum increase of 112 +/- 33% during naloxone infusion (P less than 0.05). We conclude that 1) brain or central opioid activity is not decreased in PCO; 2) increased central opioid activity does not appear to be responsible for the increased LH levels characteristic of the syndrome; and 3) decreased central dopamine activity and/or the interaction between the dopaminergic and opioid systems may be altered in PCO.


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J. D. Veldhuis, S. M. Pincus, M. C. Garcia-Rudaz, M. G. Ropelato, M. E. Escobar, and M. Barontini
Disruption of the Joint Synchrony of Luteinizing Hormone, Testosterone, and Androstenedione Secretion in Adolescents with Polycystic Ovarian Syndrome
J. Clin. Endocrinol. Metab., January 1, 2001; 86(1): 72 - 79.
[Abstract] [Full Text]




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