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Dual Secretagogue Drive of Burst-Like Growth Hormone Secretion in Postmenopausal Compared with Premenopausal Women Studied under an Experimental Estradiol Clamp

Division of Endocrinology and Metabolism (D.E., K.M., K.B., J.M.M., J.D.V.), Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905; Department of Statistics (D.M.K.), University of Virginia, Charlottesville, Virginia 22904; and Department of Medicine (C.Y.B.), Tulane University Health Sciences Center, New Orleans, Louisiana 70112

Address all correspondence and requests for reprints to: Dr. Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905. E-mail: veldhuis.johannes{at}mayo.edu

We show that in an experimentally enforced estradiol-predominant milieu, postmenopausal compared with premenopausal women maintain 1) decreased fasting GH and IGF-I concentrations, 2) reduced basal and pulsatile GH secretion, and 3) attenuated GH secretion after maximal stimulation by the paired secretagogues L-arginine/GH-releasing peptide (GHRP)-2, L-arginine/GHRH, and GHRP-2/GHRH. These foregoing outcomes are selective, because menopausal status did not determine mean GH secretory-burst frequency or peptide-induced waveform shortening. Abdominal visceral fat mass predicted up to 25% of the variability in fasting and stimulated GH secretion in the combined cohorts under fixed systemic estradiol availability. Accordingly, as much as three-fourths of interindividual differences in burst-like GH secretion among healthy pre- and postmenopausal women arise from age-related mechanisms independently of short-term systemic estrogen availability and relative intraabdominal adiposity.

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