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Am J Physiol Endocrinol Metab (January 8, 2002). doi:10.1152/ajpendo.00537.2001
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Articles in PresS, published online ahead of print January 8, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00537.2001
Submitted on December 3, 2001
Accepted on December 31, 2001

Pulsatile Growth Hormone Secretion Persists in Genetic Growth Hormone Releasing Hormone Resistance

Hiralal G Maheshwari1, Suzan S Pezzoli2, Asad Rahim3, Stephen M Shalet3, Michael O Thorner2, and Gerhard Baumann1*

1 Medicine, Northwestern University, Chicago, IL, USA
2 Internal Medicine, University of Virginia, Charlottesville, VA, USA
3 Endocrinology, Christie Hospital, Manchester, United Kingdom

* To whom correspondence should be addressed. E-mail: gbaumann{at}northwestern.edu.

Growth hormone (GH) secretion is regulated by GH releasing hormone (GHRH), somatostatin, and possibly ghrelin, but uncertainty remains about the relative contributions of these hypophysiotropic factors to GH pulsatility. Patients with genetic GHRH receptor (GHRH-R) deficiency present an opportunity to examine GH secretory dynamics in the selective absence of GHRH input. We studied circadian GH profiles in four young men homozygous for a null mutation in the GHRH-R gene, using an ultrasensitive GH assay. Residual GH secretion was pulsatile, with normal pulse frequency, but severely reduced amplitude (<1% normal) and greater than normal process disorder (as assessed by ApEn). Nocturnal GH secretion, both basal and pulsatile, was enhanced compared to day time. We conclude that rhythmic GH secretion persists in an amplitude-miniaturized version in the absence of a GHRH-R signal. The nocturnal enhancement of GH secretion is likely mediated by decreased somatostatin tone. Pulsatility of residual GH secretion may be caused by oscillations in somatostatin and/or ghrelin; it may also reflect intrinsic oscillations in somatotropes.




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