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This Article Full Text Full Text (PDF) All Versions of this Article: 285/1/E163    most recent 00334.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Dimaraki, E. V. Articles by Barkan, A. L. Search for Related Content PubMed PubMed Citation Articles by Dimaraki, E. V. Articles by Barkan, A. L.

Pulsatile and nocturnal growth hormone secretions in men do not require periodic declines of somatostatin

¹Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Michigan, and ²Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48109; ³Department of Internal Medicine, Division of Endocrinology and Metabolism, Tulane University, New Orleans, Louisiana 70112; and ⁴Novartis Pharma Ltd., CH-4002 Basel, Switzerland

Submitted 24 July 2002 ; accepted in final form 23 March 2003

Using a continuous subcutaneous octreotide infusion to create constant supraphysiological somatostatinergic tone, we have previously shown that growth hormone (GH) pulse generation in women is independent of endogenous somatostatin (SRIH) declines. Generalization of these results to men is problematic, because GH regulation is sexually dimorphic. We have therefore studied nine healthy young men (age 26 ± 6 yr, body mass index 23.3 ± 1.2 kg/m²) during normal saline and octreotide infusion (8.4 µg/h) that provided stable plasma octreotide levels (764.5 ± 11.6 pg/ml). GH was measured in blood samples obtained every 10 min for 24 h. Octreotide suppressed 24-h mean GH by 52 ± 13% (P = 0.016), GH pulse amplitude by 47 ± 12% (P = 0.012), and trough GH by 39 ± 12% (P = 0.030), whereas GH pulse frequency and the diurnal rhythm of GH secretion remained essentially unchanged. The response of GH to GH-releasing hormone (GHRH) was suppressed by 38 ± 15% (P = 0.012), but the GH response to GH-releasing peptide-2 was unaffected. We conclude that, in men as in women, declines in hypothalamic SRIH secretion are not required for pulse generation and are not the cause of the nocturnal augmentation of GH secretion. We propose that GH pulses are driven primarily by GHRH, whereas ghrelin might be responsible for the diurnal rhythm of GH.

somatotropin; pulsatility; diurnal rhythm; octreotide; ghrelin; somatotropin-releasing hormone

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