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    Pulsatile growth hormone secretion persists in genetic growth hormone-releasing hormone resistance.

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    Authors
    Maheshwari, Hiralal G
    Pezzoli, Suzan S
    Rahim, Asad
    Shalet, Stephen M
    Thorner, Michael O
    Baumann, Gerhard
    Affiliation
    Center for Endocrinology, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Medical School, and Veterans Administration Chicago Health System, Lakeside Division, Chicago, Illinois 60611, USA.
    Issue Date
    2002-04
    
    Metadata
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    Abstract
    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 by use of 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 approximate entropy). Nocturnal GH secretion, both basal and pulsatile, was enhanced compared with daytime. 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.
    Citation
    Pulsatile growth hormone secretion persists in genetic growth hormone-releasing hormone resistance. 2002, 282 (4):E943-51 Am. J. Physiol. Endocrinol. Metab.
    Journal
    American Journal of Physiology. Endocrinology and Metabolism
    URI
    http://hdl.handle.net/10541/80055
    DOI
    10.1152/ajpendo.00537.2001
    PubMed ID
    11882517
    Type
    Article
    Language
    en
    ISSN
    0193-1849
    ae974a485f413a2113503eed53cd6c53
    10.1152/ajpendo.00537.2001
    Scopus Count
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