{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T06:25:35Z","timestamp":1773296735534,"version":"3.50.1"},"reference-count":34,"publisher":"Oxford University Press (OUP)","issue":"1","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Estrogen stimulates pulsatile secretion of GH, via mechanisms that are largely unknown. An untested hypothesis is that estradiol (E<jats:sub>2<\/jats:sub>) drives GH secretion by amplifying interactions among GH-releasing hormone (GHRH), somatostatin (SS), and GH-releasing peptide (GHRP).<\/jats:p><\/jats:sec><jats:sec><jats:title>Design<\/jats:title><jats:p>The design comprised double-blind randomized prospective administration of transdermal E<jats:sub>2<\/jats:sub>vs placebo to healthy postmenopausal women (<jats:italic>n<\/jats:italic>=24) followed by pulsatile GHRH or SS infusions for 13\u200ah overnight with or without continuous GHRP2 stimulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>End points were mean concentrations, deconvolved secretion, and approximate entropy (ApEn; a regularity measure) of GH.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>By generalized ANOVA models, it was observed that E<jats:sub>2<\/jats:sub>vs placebo supplementation: i) augmented mean (13-h) GH concentrations (<jats:italic>P<\/jats:italic>=0.023), GHRH-induced pulsatile GH secretion over the first 3\u200ah (<jats:italic>P<\/jats:italic>=0.0085) and pulsatile GH secretion over the next 10\u200ah (<jats:italic>P<\/jats:italic>=0.054); ii) increased GHRP-modulated (<jats:italic>P<\/jats:italic>=0.022) and SS-modulated (<jats:italic>P<\/jats:italic>&lt;0.001) GH ApEn; and iii) did not amplify GHRH\/GHRP synergy during pulsatile GH secretion. By linear regression, E<jats:sub>2<\/jats:sub>concentrations were found to be positively correlated with GH secretion during GHRP2 infusion (<jats:italic>P<\/jats:italic>=0.022), whereas BMI was found to be negatively correlated with GH secretion during GHRH (<jats:italic>P<\/jats:italic>=0.006) and combined GHRH\/GHRP (<jats:italic>P<\/jats:italic>=0.015) stimulation. E<jats:sub>2<\/jats:sub>and BMI jointly determined triple (combined<jats:sc>l<\/jats:sc>-arginine, GHRH, and GHRP2) stimulation of GH secretion after saline (<jats:italic>R<\/jats:italic><jats:sup>2<\/jats:sup>=0.44 and<jats:italic>P<\/jats:italic>=0.003) and pulsatile GHRH (<jats:italic>R<\/jats:italic><jats:sup>2<\/jats:sup>=0.39 and<jats:italic>P<\/jats:italic>=0.013) infusions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In summary, in postmenopausal women, E<jats:sub>2<\/jats:sub>supplementation augments the amount (mass) and alters the pattern (regularity) of GH secretion via interactions among GHRH, SS, GHRP, and BMI. These outcomes introduce a more complex model of E<jats:sub>2<\/jats:sub>supplementation in coordinating GH secretion in aging women.<\/jats:p><\/jats:sec>","DOI":"10.1530\/eje-13-0733","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T13:31:20Z","timestamp":1381498280000},"page":"121-129","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":11,"title":["Estradiol regulates GH-releasing peptide's interactions with GH-releasing hormone and somatostatin in postmenopausal women"],"prefix":"10.1093","volume":"170","author":[{"given":"Catalina","family":"Norman","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nanette L","family":"Rollene","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dana","family":"Erickson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John M","family":"Miles","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cyril Y","family":"Bowers","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johannes D","family":"Veldhuis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","reference":[{"issue":"6","key":"1_12258169","doi-asserted-by":"publisher","first-page":"1102","DOI":"10.1210\/jcem-34-6-1102","volume":"34","author":"CARLSON","year":"1972","journal-title":"Journal of Clinical Endocrinology &amp; 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