The present study tests the hypothesis that estradiol (E2), compared with placebo (Pl), amplifies combined-secretagogue stimulation of GH secretion in premenopausal women studied at comparable IGF-I and testosterone concentrations. To this end, 13 women underwent GnRH agonist-induced gonadal down-regulation followed by graded transdermal add-back of E2 or Pl and randomly ordered iv infusions of saline or paired secretagogues on separate morning fasting. GH secretion was assessed by frequent blood sampling, immunochemiluminometry, and variable-waveform deconvolution analysis. Two-way ANOVA revealed that specific secretagogue combination (P < 0.001), E 2 status (P = 0.012), and their interaction (P = 0.038) jointly determined GH secretory-burst mass. Compared with Pl, the E2-clamped milieu elevated mean fasting GH concentrations (P = 0.032), the mass of GH secreted in bursts (P = 0.037), and maximal stimulation by paired L-arginine/GH-releasing peptide (GHRP)-2 (P = 0.028). E2 also markedly accelerated the initial release of GH induced by GHRH/GHRP-2 (P < 0.001) and L-arginine/GHRH (P < 0.01). By linear regression analysis, E 2 concentrations positively forecast 41% of intersubject variability in GH secretion stimulated by combined L-arginine/GHRP-2 (P = 0.018), whereas abdominal visceral-fat mass negatively predicted 49% of that due to L-arginine/GHRH (P = 0.012). These data indicate that pulsatile GH secretion in young women studied at constant IGF-I and testosterone concentrations is dictated 3-fold jointly by secretagogue pair, E2 availability, and intraabdominal adiposity. Moreover, the rapidity of GH release is controlled 2-fold jointly by E2 and GHRH.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical