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Submitted on December 15, 2005
Accepted on March 3, 2006
Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, MN 55905; Endocrine Section, Department of Medicine, Salem Veterans Affairs Medical Center, Salem, VA 24153; 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.
Context. Ghrelin is 28 amino acid Ser3-octanoylated peptide that stimulates GH secretion in vivo and in vitro. Beyond the capability of ghrelin to synergize with GHRH, little is known about multipeptide modulation of ghrelin's actions in the human.
Objective. To test the hypothesis that ghrelin can stimulate GH secretion in the absence or presence of somatostatin withdrawal (induced by L-arginine infusion) and stress-like drive by CRH (CRH).
Design. Randomized, double-blind, placebo-controlled crossover interventional study.
Setting. Academic medical center.
Participants. Nine healthy postmenopausal women not receiving sex hormones.
Interventions. Intravenous infusion of saline or human with L-arginine or hum n CRH followed by bolus iv injection of ghrelin.
Outcome Measures. Pulsatile GH secretion quantified by repetitive blood sampling, immunochemiluminometry and deconvolution analysis.
Results. Consecutive saline/ghrelin infusion increased pulsatile GH secretion (µg/L/3 h) [mean ± SEM] from 2.7 ± 1.0 (saline/saline) to 20 ± 5.0 [P < 0.01]. The magnitude of the effect of L-arginine/saline was comparable at 20 ± 4.5 [P < 0.01]. In contrast, sequential L-arginine/ghrelin evoked true synergy of GH release, 93 ± 14 [P = 0.003 vs. L-arginine alone and P = 0.008 vs. ghrelin alone]. Human CRH did not affect GH responses to saline/saline (3.9 ± 1.1), saline/ghrelin (19 ± 3.3), L-arginine/saline (16 ± 2.7) or L-arginine/ghrelin (90 ± 13).
Conclusions. Assuming that L-arginine reduces somatostatin outflow, we infer that ghrelin can activate hypothalamopituitary pathways that are both dependent upon and independent of somatostatinergic restraint even in the face of a strong stress-related signal.
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