| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Internal Medicine (S.K.J., E.V.D., A.L.B.), Division of Endocrinology and Metabolism, University of Michigan Medical Center, and Department of Veterans Affairs Medical Center (K.V.S., A.L.B.), Ann Arbor, Michigan 48109
Address all correspondence and requests for reprints to: Ariel L. Barkan, M.D., University of Michigan Medical Center, 3920 Taubman Center, Box 0354, Ann Arbor, Michigan 48109-0354. E-mail: abarkan{at}umich.edu.
GH secretory patterns in humans are sexually dimorphic in terms of pulse regularity, amplitude of the diurnal rhythm, and magnitude of basal (trough) secretion. The neuroendocrine mechanisms of gender-specific GH regulation in humans are currently unknown, but the interpulse GH levels are generally assumed to be controlled by somatostatin. In rats, however, administration of antiserum to GHRH lowers GH interpulse levels in females but not males. In this study, using a competitive antagonist to GHRH in humans, we investigated whether endogenous GHRH has differential, gender-specific effects on the interpulse GH levels. Six healthy men and five healthy women (20–28 yr old) who were nonobese, did not smoke, and were on no medications known to influence GH secretion were studied. Each served as his or her own control during an infusion of GHRH antagonist or saline for a 27-h period. A control bolus of GHRH was given near the end of the infusion. In both sexes during GHRH antagonist infusion, mean GH, pulse amplitude, and GH response to GHRH decreased significantly, whereas pulse frequency remained unchanged. However, during the GHRH antagonist infusion, trough GH did not significantly change in men (P = 0.54) but significantly decreased in women (P = 0.008). Deconvolution analysis confirmed the lack of a significant change in basal secretion in men (P = 0.81) as opposed to women (P = 0.006). We conclude that sexual dimorphism in the neuroendocrine regulation of GH secretion in humans involves a differential role of endogenous GHRH in maintaining baseline GH.
This work was supported by the Endocrine Fellowship Foundation Grant (to S.K.J.); a Veterans Affairs Medical Research Service grant (to A.L.B.); and National Institutes of Health Grant MO1-RR-00042 (General Clinical Research Center).
Abbreviation: SRIF, Somatostatin.
This article has been cited by other articles:
 |
|
 |
|
  R. M. Luque and R. D. Kineman Gender-Dependent Role of Endogenous Somatostatin in Regulating Growth Hormone-Axis Function in Mice Endocrinology, December 1, 2007; 148(12): 5998 - 6006. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Alba and R. Salvatori A Mouse with Targeted Ablation of the Growth Hormone-Releasing Hormone Gene: A New Model of Isolated Growth Hormone Deficiency Endocrinology, September 1, 2004; 145(9): 4134 - 4143. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Racine, K. V. Symons, C. M. Foster, and A. L. Barkan Augmentation of Growth Hormone Secretion after Testosterone Treatment in Boys with Constitutional Delay of Growth and Adolescence: Evidence against an Increase in Hypothalamic Secretion of Growth Hormone-Releasing Hormone J. Clin. Endocrinol. Metab., July 1, 2004; 89(7): 3326 - 3331. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-O. Jansson and J. Svensson Growth Hormone (GH) Replacement in Women in Relation to Their Endogenous GH Secretion J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 3066 - 3066. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
