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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/E483    most recent 00136.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Veldhuis, J. D. Articles by Erickson, D. PubMed PubMed Citation Articles by Veldhuis, J. D. Articles by Erickson, D.

Regulation of basal, pulsatile, and entropic (patterned) modes of GH secretion in a putatively low-somatostatin milieu in women

Departments of ¹Internal Medicine and ²Obstetrics and Gynecology, Mayo Medical and Graduate Schools of Medicine, Mayo Clinic, Rochester, Minnesota

Submitted 2 March 2009 ; accepted in final form 2 June 2009

Somatostatin (SS) released by hypothalamic neurons inhibits GH exocytosis noncompetitively. Therefore, we postulated that attenuation of GH feedback-induced SS outflow would help to unmask covariates of endogenous secretagogue drive. To this end, 42 healthy pre- and postmenopausal women were randomly assigned to receive leuprolide plus estradiol (E₂) or leuprolide plus placebo. A putatively low-SS milieu was imposed by L-arginine infusion. Deconvolution and regularity analyses were applied to 6-h GH concentration-time profiles. By two-way ANOVA, age negatively (P < 0.001) and E₂ positively (P = 0.001) determined pulsatile GH secretion in the presumptively SS-deficient milieu (P < 0.001). Comparable effects were exerted on the mass of GH secreted per burst per unit distribution volume (age P = 0.001, E₂ P < 0.001, overall P < 0.001). E₂ alone predicted basal (nonpulsatile) GH secretion (P = 0.004). Stepwise forward-selection multivariate regression demonstrated that age (P = 0.0017) and E₂ (P = 0.0002) together explained 46% of intersubject variability in pulsatile GH secretion (P < 0.001) and fully replaced the negative univariate effect of abdominal visceral fat (r² = 0.32, P < 0.001). Moreover, age and E₂ (but not AVF) interacted to supervise GH regularity (P = 0.007). We conclude that age and E₂ availability individually and together constitute primary predictors of basal, pulsatile, and patterned GH secretion in an inferentially feedback-silenced context in healthy women. Therefore, both factors must be considered in framing hypotheses of endogenous GH drive.

growth hormone; somatotropin; insulin-like growth factor I; female; pituitary