Arginine Reinstates the Somatotrope Responsiveness to Intermittent Growth Hormone-Releasing Hormone Administration in Normal Adults (original) (raw)
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Research Articles| April 07 2008
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
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Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Division of Endocrinology, Department of Clinical Physiopathology, University of Turin, Italy
Search for other works by this author on:
Neuroendocrinology (1991) 54 (3): 291–294.
Received:
October 22 1990
Accepted:
January 31 1991
Published Online:
April 07 2008
Abstract
It is well known that in normal adults the growth hormone (GH) response to GH-releasing hormone (GHRH) is inhibited by previous administration of the neurohormone. In 7 healthy volunteers (age 20–34 years) we studied the GH responses to two consecutive GHRH boluses (1 µg/kg i.v. every 120 min) alone or coadministered with arginine (30 g i.v. over 30 min). The GH response to the first GHRH bolus (area under the curve, mean ± SEM: 506.3 ± 35.1 µg/l/h) was higher (p = 0.0001) than that to the second one (87.1 ± 14.6 µg/l/h). The latter response was clearly increased (p = 0.0001) by coadministering arginine (980.5 ± 257.5 µg/l/h). When every GHRH bolus was combined with arginine a marked potentiation of GH response to both boluses was found. However, the second combined administration of arginine and GHRH induced a GH increase which was lower compared to the first one (p = 0.016). In conclusion, our results show that arginine potentiates the GHRH-induced GH secretion preventing the lessening of somatotrope responsiveness to the neurohormone alone. As there is evidence that this phenomenon is due to an enhanced somatostatin release, these findings give further evidence of a somatostatin-suppressing effect of arginine.
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© 1991 S. Karger AG, Basel
1991
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