In Vivo Actions of a Gonadotropin-Releasing Hormone (GnRH) Antagonist on Gonadotropin-II and Growth Hormone Secretion in Goldfish, Carassius auratus

1994 ◽  
Vol 96 (3) ◽  
pp. 427-437 ◽  
Author(s):  
C.K. Murthy ◽  
W. Zheng ◽  
V.L. Trudeau ◽  
C.S. Nahorniak ◽  
J.E. Rivier ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Carassius Auratus ◽  
Gnrh Antagonist ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Goldfish Carassius Auratus ◽  
Gonadotropin Ii

scholarly journals Effects of Growth Hormone-Releasing Hormone (GRF) Analogs, Bovine and Rat GRF on Growth Hormone Secretion in Cattle In Vivo.

1997 ◽  
Vol 44 (6) ◽  
pp. 811-817 ◽  
Author(s):  
TSUTOMU HASHIZUME ◽  
KENJI OHTSUKI ◽  
KOICHI SASAKI ◽  
MASAZUMI YANAGIMOTO ◽  
HIROSHI MASUDA ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone

scholarly journals AMPK-Dependent Mechanisms but Not Hypothalamic Lipid Signaling Mediates GH-Secretory Responses to GHRH and Ghrelin

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1940
Author(s):  
María J. Vázquez ◽  
Marta G. Novelle ◽  
Francisca Rodríguez-Pacheco ◽  
Ricardo Lage ◽  
Luis Varela ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Hormone Secretion ◽  
Mammalian Target Of Rapamycin ◽  
Growth Hormone Secretion ◽  
Lipid Signaling ◽  
Energy Status ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone

GH (growth hormone) secretion/action is modulated by alterations in energy homeostasis, such as malnutrition and obesity. Recent data have uncovered the mechanism by which hypothalamic neurons sense nutrient bioavailability, with a relevant contribution of AMPK (AMP-activated protein kinase) and mTOR (mammalian Target of Rapamycin), as sensors of cellular energy status. However, whether central AMPK-mediated lipid signaling and mTOR participate in the regulation of pituitary GH secretion remains unexplored. We provide herein evidence for the involvement of hypothalamic AMPK signaling, but not hypothalamic lipid metabolism or CPT-1 (carnitine palmitoyltransferase I) activity, in the regulation of GH stimulatory responses to the two major elicitors of GH release in vivo, namely GHRH (growth hormone–releasing hormone) and ghrelin. This effect appeared to be GH-specific, as blocking of hypothalamic AMPK failed to influence GnRH (gonadotropin-releasing hormone)-induced LH (luteinizing hormone) secretion. Additionally, central mTOR inactivation did not alter GH responses to GHRH or ghrelin, nor this blockade affected LH responses to GnRH in vivo. In sum, we document here for the first time the indispensable and specific role of preserved central AMPK, but not mTOR, signaling, through a non-canonical lipid signaling pathway, for proper GH responses to GHRH and ghrelin in vivo.

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