TY - JOUR
T1 - Arginine abolishes the inhibitory effect of glucose on the growth hormone response to growth hormone-releasing hormone in man
AU - Ghigo, E.
AU - Miola, C.
AU - Aimaretti, G.
AU - Valente, F.
AU - Procopio, M.
AU - Arvat, E.
AU - Yin-Zhang, W.
AU - Camanni, F.
N1 - Funding Information:
From the Division of Endocrinology, Depantnent of Clinical Pathophysioto6y, University of Turin, Italy. Supported by grants of the Minister0 dell’ Universita e Ricerca Scientifica e Tecnologica. Address reprint requests to F. Camanni, MD, Divisione di Endocri-nologia, Ospedale Molinette, C.so Dogliotti, 14, 10126 Totino, Italia. Copyright 0 1992 by W.B . Saunders Company 0026-0495/92/4109-0012$03.OOiO
PY - 1992/9
Y1 - 1992/9
N2 - Acute hyperglycemia inhibits the growth hormone (GH) response to several stimuli including growth hormone-releasing hormone (GHRH), likely acting by stimulation of endogenous somatostatin release. The aim of our study was to verify whether arginine ([Arg] 30 g intravenously [IV] in 30 minutes), a well-known GH secretagogue likely acting via inhibition of hypothalamic somatostatin release, counteracts the inhibitory effect of oral glucose (OG) administration (100 mg orally) on the GH response to GHRH (1 μg/kg IV bolus) in seven normal subjects (aged 20 to 30 years). The GH response to GHRH (peak, 11.6 ± 1.8 μg/L) was inhibited by previous OG load (peak, 7.4 ± 0.8 μg/L; P < .02 v GHRH alone) and potentiated by Arg coadministration (peak, 36.2 ± 8.8 μg/L; P < .03 v GHRH alone). The potentiating effect of Arg on the GHRH-induced GH increase was unaffected by previous OG load (peak, 30.4 ± 6.9 μg/L). In conclusion, our results show that Arg abolishes the inhibitory effect of OG administration on the GHRH-induced GH response in man. These data, although indirect, suggest that both acute hyperglycemia and Arg act at the hypothalamic level, stimulating and inhibiting, respectively, the release of somatostatin.
AB - Acute hyperglycemia inhibits the growth hormone (GH) response to several stimuli including growth hormone-releasing hormone (GHRH), likely acting by stimulation of endogenous somatostatin release. The aim of our study was to verify whether arginine ([Arg] 30 g intravenously [IV] in 30 minutes), a well-known GH secretagogue likely acting via inhibition of hypothalamic somatostatin release, counteracts the inhibitory effect of oral glucose (OG) administration (100 mg orally) on the GH response to GHRH (1 μg/kg IV bolus) in seven normal subjects (aged 20 to 30 years). The GH response to GHRH (peak, 11.6 ± 1.8 μg/L) was inhibited by previous OG load (peak, 7.4 ± 0.8 μg/L; P < .02 v GHRH alone) and potentiated by Arg coadministration (peak, 36.2 ± 8.8 μg/L; P < .03 v GHRH alone). The potentiating effect of Arg on the GHRH-induced GH increase was unaffected by previous OG load (peak, 30.4 ± 6.9 μg/L). In conclusion, our results show that Arg abolishes the inhibitory effect of OG administration on the GHRH-induced GH response in man. These data, although indirect, suggest that both acute hyperglycemia and Arg act at the hypothalamic level, stimulating and inhibiting, respectively, the release of somatostatin.
UR - http://www.scopus.com/inward/record.url?scp=0026744593&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(92)90127-V
DO - 10.1016/0026-0495(92)90127-V
M3 - Article
SN - 0026-0495
VL - 41
SP - 1000
EP - 1003
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 9
ER -
