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Submitted on September 2, 2004
Accepted on December 9, 2004
Department of Statistics, Department of Internal Medicine, University of Virginia, Charlottesville, VA 22908; Department of Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112
* To whom correspondence should be addressed. E-mail: veldhuis.johannes{at}mayo.edu.
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 (Te) concentrations. To this end, 13 women underwent GnRH agonist-induced gonadal downregulation followed by graded transdermal addback of E2 or Pl and randomly ordered iv infusions of saline or paired secretagogues on separate mornings 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), E2 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/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, E2 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 Te concentrations is dictated threefold jointly by secretagogue pair, E2 availability and intraabdominal adiposity. Moreover, the rapidity of GH release is controlled twofold jointly by E2 and GHRH.
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