Inhibitory Effect of Amylin on Growth Hormone Responsiveness to Growth-Hormone-Releasing Hormone in the Rat

1995 ◽  
Vol 62 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Carmela Netti ◽  
Valeria Sibilia ◽  
Francesca Pagani ◽  
Norma Lattuada ◽  
Mariella Coluzzi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Hormone Responsiveness

GALANIN ABOLISHES THE INHIBITORY EFFECT OF CHOLINERGIC BLOCKADE ON GROWTH HORMONE-RELEASING HORMONE-INDUCED SECRETION OF GROWTH HORMONE IN MAN

1988 ◽  
Vol 116 (3) ◽  
pp. R1-R2 ◽  
Author(s):  
V.K.K. Chatterjee ◽  
J.A. Ball ◽  
C. Proby ◽  
J.M. Burrin ◽  
S.R. Bloom
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Normal Male ◽  
Growth Hormone Releasing Hormone ◽  
Maximal Dose ◽  
Muscarinic Antagonist ◽  
Releasing Hormone ◽  
Cholinergic Pathways ◽  
Cholinergic Blockade ◽  
Male Volunteers

ABSTRACT In five healthy normal male volunteers, pretreatment with the cholinergic muscarinic antagonist pirenzepine (30 mg i.v.) almost abolished the growth hormone (GH) response to a maximal dose (120 μg i.v.) of growth hormone-releasing hormone (GHRH) (GH response at 40 min 5.6 ± 1.3 mU/l with GHRH and pirenzepine vs 40.8 ± 5.3 mU/l with GHRH alone, P <0.02). Concomitant i.v. infusion of galanin (40 pmol/kg/min) with pirenzepine not only restored but significantly potentiated the GH response to GHRH (GH at 40 min 72.2 ± 10.5 mU/l, P <0.001 vs GHRH and pirenzepine, P <0.02 vs GHRH alone). Previous studies have proposed that cholinergic pathways control GH release via samatostatin and this study suggests that galanin may act by modulating hypothalamic somatostatinergic tone either directly or, possibly, by facilitating cholinergic neurotransmission.

scholarly journals The role of pit-1 in the regulation of the rat growth hormone-releasing hormone receptor gene transcription by glucocorticoids

2005 ◽  
Vol 35 (3) ◽  
pp. 477-488 ◽  
Author(s):  
Haruo Nogami ◽  
Yoshiki Hiraoka ◽  
Kiyomoto Ogasawara ◽  
Sadakazu Aiso ◽  
Setsuji Hisano
Keyword(s):  
Growth Hormone ◽  
Gene Transcription ◽  
Receptor Gene ◽  
Inhibitory Effect ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Proper Distance ◽  
Ghrh Receptor ◽  
Rat Growth

Glucocorticoids are involved in the regulation of the rat growth hormone-releasing hormone (GHRH) receptor gene expression, but they act only in the presence of the pituitary specific transcription factor, pit-1. In this study, the role of pit-1 in the glucocorticoid stimulation of the GHRH-receptor gene transcription was examined. The results suggest the presence of a silencer element in the promoter and it is postulated that pit-1 permits glucocorticoid action through suppressing the inhibitory effect of an as yet unknown factor that binds to this element. The present results also suggest that the synergistic activation of the rat GHRH-receptor gene transcription depends on the proper distance between the proximal glucocorticoid response element and the pit-1 binding site.

scholarly journals Growth hormone-releasing hormone receptor antagonists inhibit human gastric cancer through downregulation of PAK1–STAT3/NF-κB signaling

2016 ◽  
Vol 113 (51) ◽  
pp. 14745-14750 ◽  
Author(s):  
Jinfeng Gan ◽  
Xiurong Ke ◽  
Jiali Jiang ◽  
Hongmei Dong ◽  
Zhimeng Yao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Hormone ◽  
Cell Lines ◽  
Cultured Cells ◽  
Nuclear Factor Κb ◽  
Inhibitory Effect ◽  
Human Gastric Cancer ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
P21 Activated Kinase

Gastric cancer (GC) ranks as the fourth most frequent in incidence and second in mortality among all cancers worldwide. The development of effective treatment approaches is an urgent requirement. Growth hormone-releasing hormone (GHRH) and GHRH receptor (GHRH-R) have been found to be present in a variety of tumoral tissues and cell lines. Therefore the inhibition of GHRH-R was proposed as a promising approach for the treatment of these cancers. However, little is known about GHRH-R and the relevant therapy in human GC. By survival analyses of multiple cohorts of GC patients, we identified that increased GHRH-R in tumor specimens correlates with poor survival and is an independent predictor of patient prognosis. We next showed that MIA-602, a highly potent GHRH-R antagonist, effectively inhibited GC growth in cultured cells. Further, this inhibitory effect was verified in multiple models of human GC cell lines xenografted into nude mice. Mechanistically, GHRH-R antagonists target GHRH-R and down-regulate the p21-activated kinase 1 (PAK1)-mediated signal transducer and activator of transcription 3 (STAT3)/nuclear factor-κB (NF-κB) inflammatory pathway. Overall, our studies establish GHRH-R as a potential molecular target in human GC and suggest treatment with GHRH-R antagonist as a promising therapeutic intervention for this cancer.

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