| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Endocrine Research Unit, Department of Internal Medicine, Mayo School of Graduate Medical Education, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota; 2Departments of Bioethics and Statistics, University of Virginia, Charlottesville; and 3Endocrine Service, Research and Development, Salem Veterans Affairs Medical Center, Salem, Virginia
Submitted 31 August 2004 ; accepted in final form 17 November 2004
Testosterone (Te) concentrations fall gradually in healthy aging men. Postulated mechanisms include relative failure of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), and/or gonadal Te secretion. Available methods to test Leydig cell Te production include pharmacological stimulation with human chorionic gonadotropin (hCG). We reasoned that physiological lutropic signaling could be mimicked by pulsatile infusion of recombinant human (rh) LH during acute suppression of LH secretion. To this end, we studied eight young (ages 19–30 yr) and seven older (ages 61–73 yr) men in an experimental paradigm comprising 1) inhibition of overnight LH secretion with a potent selective GnRH-receptor antagonist (ganirelix, 2 mg sc), 2) intravenous infusion of consecutive pulses of rh LH (50 IU every 2 h), and 3) chemiluminometric assay of LH and Te concentrations sampled every 10 min for 26 h. Statistical analyses revealed that 1) ganirelix suppressed LH and Te equally (> 75% median inhibition) in young and older men, 2) infused LH pulse profiles did not differ by age, and 3) successive intravenous pulses of rh LH increased concentrations of free Te (ng/dl) to 4.6 ± 0.38 (young) and 2.1 ± 0.14 (older; P < 0.001) and bioavailable Te (ng/dl) to 337 ± 20 (young) and 209 ± 16 (older; P = 0.002). Thus controlled pulsatile rh LH drive that emulates physiological LH pulses unmasks significant impairment of short-term Leydig cell steroidogenesis in aging men. Whether more prolonged pulsatile LH stimulation would normalize this inferred defect is unknown.
luteinizing hormone; Leydig cell; aging; male; human
This article has been cited by other articles:
|
|
 |
|
  A. Cailleux-Bounacer, Y. Reznik, B. Cauliez, J. F. Menard, C. Duparc, and J. M. Kuhn Evaluation of endocrine testing of Leydig cell function using extractive and recombinant human chorionic gonadotropin and different doses of recombinant human LH in normal men Eur. J. Endocrinol., August 1, 2008; 159(2): 171 - 178. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Lacombe, V. Lelievre, C. E. Roselli, W. Salameh, Y.-h. Lue, G. Lawson, J.-M. Muller, J. A. Waschek, and E. Vilain Delayed testicular aging in pituitary adenylate cyclase-activating peptide (PACAP) null mice PNAS, March 7, 2006; 103(10): 3793 - 3798. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Y. Liu, S. M. Pincus, P. Y. Takahashi, P. D. Roebuck, A. Iranmanesh, D. M. Keenan, and J. D. Veldhuis Aging attenuates both the regularity and joint synchrony of LH and testosterone secretion in normal men: analyses via a model of graded GnRH receptor blockade Am J Physiol Endocrinol Metab, January 1, 2006; 290(1): E34 - E41. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Y. Liu, P. Y. Takahashi, P. D. Roebuck, A. Iranmanesh, and J. D. Veldhuis Age-specific changes in the regulation of LH-dependent testosterone secretion: assessing responsiveness to varying endogenous gonadotropin output in normal men Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2005; 289(3): R721 - R728. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
