Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal hyperandrogenism is a common feature of patients with polycystic ovary syndrome (PCO). This may be due to enhanced adrenal sensitivity to ACTH. Because enhanced ovarian androgen secretion does not appear to explain this phenomenon, we explored the role of estrogen in inducing enhanced adrenal sensitivity, in that a state of relative hyperestrogenism exists in PCO. Eight patients with PCO and seven matched controls received ovine corticotropin-releasing hormone (oCRH; 0.1 micrograms/kg) iv before and after hypoestrogenism was induced by leuprolide acetate (LA; 1 mg, sc, each day). In patients with PCO, a third oCRH test was repeated after transdermal estradiol (E2; 0.1 mg) had been applied for a week, during which time LA was continued. At baseline, patients with PCO had increased responses of 11 beta-hydroxyandrostenedione and dehydroepiandrosterone (P < 0.03 and P < 0.02) and increased delta maximal ratios of androstenedione (A4)/ACTH and dehydroepiandrosterone/ACTH (P < 0.01) after oCRH treatment. After LA administration to patients with PCO, these ratios were significantly suppressed (P < 0.01) and returned to baseline after E2 was added. There were no changes in controls. Steroid ratio responses to oCRH suggested that 17,20-desmolase activity (delta maximum change in the ratio of A4/17-hydroxyprogesterone) was lowered with estrogen suppression and increased again after transdermal E2 administration. There was a significant positive correlation between changes in E2 levels and delta maximum change in the ratios of A4/17-OHP after oCRH treatment, signifying 17,20-desmolase activity (r = 0.58, P < 0.02). In conclusion, these data provide evidence that estrogen is at least one factor that influences adrenal androgen sensitivity in PCO and may help explain the frequent finding of adrenal hyperandrogenism in this syndrome.
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PMID:The impact of estrogen on adrenal androgen sensitivity and secretion in polycystic ovary syndrome. 785 27

The adrenal response to adrenocorticotropic hormone (ACTH) stimulation and dexamethasone (DEX) inhibition tests in six healthy ovulatory control women (31.6 +/- SD 0.6 years old) with a body mass index (BMI) of 24.8 +/- 1.3 kg/m2 (Group 1) were compared against seven women (28.1 +/- 0.8 years old, BMI 30.9 +/- 2.1 kg/m2) with polycystic ovary syndrome (PCOS) and hyperinsulinism (Group 2). In both groups the following tests were performed: a) a 100-g 2-h oral glucose tolerance test (OGTT) with serum glucose and insulin measurements; b) an ACTH stimulation test (2-h 0.25 mg iv bolus); and c) a 1 mg oral midnight DEX inhibition test. Assays of serum cortisol. 17-hydroxyprogesterone, dehydroepiandrosterone sulfate (DHEA-S), free testosterone (FT), and androstenedione during the ACTH and DEX tests were performed. Contrary to Group 1, Group 2 showed: a) higher basal luteinizing hormone follicle-stimulating hormone ratio, FT, and insulin, and hyperinsulinism during the OGTT; b) FT significantly higher after ACTH; and c) FT and DHEAS did not show a significant inhibition with DEX. Our results suggest a certain degree of adrenal participation in the pathogenesis of the hyperandrogenism in these women, which may be the final expression of a synergistic stimulation of the adrenals by hyperinsulinism, relatively high LH, and chronic hyperestrogenism, all of which are present virtually in all women with PCOS.
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PMID:[Androgen response in women with polycystic ovary syndrome and hyperinsulinemia during stimulation with corticotrophin and inhibition with dexamethasone]. 896 89