Trial reportThe Journal of clinical endocrinology and metabolism2008
Pituitary and/or peripheral estrogen-receptor alpha regulates follicle-stimulating hormone secretion, whereas central estrogenic pathways direct growth hormone and prolactin secretion in postmenopausal women.
Trial report in The Journal of clinical endocrinology and metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Endogenous Estrogen Regulates Somatostatin-Induced Rebound GH Secretion in Postmenopausal Women.The Journal of clinical endocrinology and metabolism · 2016Trial
- Estradiol regulates GH-releasing peptide's interactions with GH-releasing hormone and somatostatin in postmenopausal women.European journal of endocrinology · 2014Trial
- Preservation of GHRH and GH-releasing peptide-2 efficacy in young men with experimentally induced hypogonadism.European journal of endocrinology · 2009Trial
- Aromatase and 5alpha-reductase inhibition during an exogenous testosterone clamp unveils selective sex steroid modulation of somatostatin and growth hormone secretagogue actions in healthy older men.The Journal of clinical endocrinology and metabolism · 2009Trial
- Predicting radiological regression in benign breast hyperplasia: the prolactin-to-estradiol ratio as a prognostic biomarker.Frontiers in medicine · 2026Article
- Central and peripheral regulation of the GH/IGF-1 axis: GHRH and beyond.Reviews in endocrine & metabolic disorders · 2025Review
- Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions.Biomedicines · 2022Review
- Article
- Symptoms of menopause - global prevalence, physiology and implications.Nature reviews. Endocrinology · 2018Review
- Effects of Toremifene, a Selective Estrogen Receptor Modulator, on Spontaneous and Stimulated GH Secretion, IGF-I, and IGF-Binding Proteins in Healthy Elderly Subjects.Journal of the Endocrine Society · 2018Article
- Estradiol-modified prolactin secretion independently of action potentials and CaNaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Effects of fulvestrant on biological activity and Wnt expression in rat GH3 cells.Neural regeneration research · 2012Article
- Estrogen negative feedback on gonadotropin secretion: evidence for a direct pituitary effect in women.The Journal of clinical endocrinology and metabolism · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEstradiol (E(2)) stimulates GH and prolactin secretion and suppresses FSH secretion in postmenopausal women. Whether central nervous system (CNS) or pituitary mechanisms (or both) mediate such actions is not known.
objectiveOur objective was to distinguish between hypothalamic and pituitary or peripheral (hepatic) actions of E2.
settingThis study was performed in an academic medical center.
designThis was a double-blind, prospectively randomized, placebo (Pl)-controlled study.
methodsThe capability of a selective, noncompetitive, non-CNS permeant estrogen receptor (ER)-alpha antagonist, fulvestrant (FUL) to antagonize the effects of transdermal E2 and Pl on GH, prolactin, and FSH secretion was assessed in 43 women (ages 50-80 yr) in a four parallel-cohort study. Each woman received four secretagogue infusions to stimulate GH secretion. IGF-I and its binding proteins were measured secondarily.
resultsAdministration of Pl/E2 increased GH and prolactin concentrations by 100%, and suppressed FSH concentrations by more than 50% (each P<or=0.004 compared with Pl/Pl). Treatment with FUL/E2 compared with Pl/E2 partially relieved estrogen's inhibition of FSH secretion (P=0.041), without altering E2's stimulation of prolactin secretion. ANOVA further revealed that: 1) estrogen milieu (P=0.014) and secretagogue type (P<0.001) each determined GH concentrations; 2) FUL/Pl suppressed IGF-I concentrations (P<0.001); 3) FUL abrogated estrogen's elevation of IGF binding protein-1 concentrations (P<0.001); and 4) FUL did not oppose estrogen's suppression of IGF binding protein-3 concentrations (P<0.001). SUMMARY AND
conclusionsResponses to a non-CNS permeant ERalpha antagonist indicate that E2 inhibits FSH secretion in part via pituitary/peripheral ERalpha, drives prolactin output via nonpituitary/nonperipheral-ERalpha effects, and directs GH secretion and IGF-I-binding proteins by complex mechanisms.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.