NCT02026973

Impact of Endogenous E2 on SSI and GH Rebound

Impact of Endogenous Estrogen on Somatostatin Inhibition and Growth Hormone Rebound in Older Women

• Status: Completed
• Phase: Phase 1
• Study type: Interventional
• Enrollment: 62 (actual)
• Sponsor: Mayo Clinic · Academic / Other
• Sex: Female
• Age: 55 Years – 80 Years
• Healthy volunteers: Accepted

Summary

Endogenous estrogens maintain growth hormone (GH) secretion in postmenopausal women by potentiating endogenous GH-releasing hormone (GHRH) drive and restraining somatostatin inhibition of GH release.

Detailed description

Systemic concentrations of testosterone (Te), estradiol (E2), GH, IGF-I and IGFBP-3 decline in healthy aging individuals (1-3). Sex-steroid deprivation accentuates GH and IGF-I depletion, since Te and E2 stimulate GH and IGF-I production in older adults, hypogonadal patients of all ages, and patients undergoing gender reassignment (1,2,4). Tamoxifen blocks the effect of Te, suggesting involvement of E2 in GH's stimulation in men (5). E2 also stimulates GH secretion in women, putatively via the nuclear estrogen receptor (ER-alpha) (1,2,6,7). Because Te, E2 and GH fall with menopause, and Te is converted to E2 by aromatization in the body (8-10), we postulate that diminished Te concentrations, Te→E2 concentrations and low E2 mediate low GH output in older women. What remains unknown is whether the low E2 levels in postmenopausal women retain GH-stimulating effects. To test this notion would require blocking: (i) aromatase-enzyme activity, which mediates E2 synthesis from Te, and/or (ii) estrogen receptor-alpha, which transduces most of E2's stimulation of the GH axis.

Conditions

• Normal Healthy Volunteers

Interventions

Type	Name	Description
DRUG	Fulvestrant
DRUG	Anastrozole
DRUG	Placebo
DRUG	Somatostatin

Timeline

• Start date: 2014-03-01
• Primary completion: 2015-11-01
• Completion: 2015-11-01
• First posted: 2014-01-03
• Last updated: 2016-03-16

Locations

1 site across 1 country: United States