Roles of Somatostatin and Growth Hormone-Releasing Factor in Ether Stress Inhibition of Growth Hormone Release

1991 ◽  
Vol 54 (5) ◽  
pp. 515-520 ◽  
Author(s):  
Cecilia Aguila ◽  
Robert L. Pickle ◽  
Wen H. Yu ◽  
Samuel M. McCann
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Inhibition Of Growth

scholarly journals Effect of growth hormone-releasing factor (1-29)NH2 and thyrotropin-releasing factor on growth hormone release in lactating sows

1987 ◽  
Vol 27 (2B) ◽  
pp. 601-603 ◽  
Author(s):  
P. DUBREUIL ◽  
G. PELLETIER ◽  
D. PETITCLERC ◽  
H. LAPIERRE ◽  
Y. COUTURE ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Lactating Sows

Testosterone Inhibition of Growth Hormone Release Stimulated by a Growth Hormone Secretagogue

2006 ◽  
Vol 84 (2) ◽  
pp. 115-122 ◽  
Author(s):  
Antonello E. Rigamonti ◽  
Silvano G. Cella ◽  
Claudio Giordani ◽  
Sara M. Bonomo ◽  
Marialuisa Giunta ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Secretagogue ◽  
Inhibition Of Growth

Phorbol ester, not growth hormone releasing factor, consistently stimulates growth hormone release from somatotroph adenomas in culture

1991 ◽  
Vol 34 (5) ◽  
pp. 377-382 ◽  
Author(s):  
Naoya Emoto ◽  
Eiji Ohmura ◽  
Osamu Isozaki ◽  
Toshio Tsushima ◽  
Kazuo Shizume ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Phorbol Ester ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor

Altered release of growth hormone from dispersed adenohypophysial cells of streptozotocin diabetic rats. II. Effects of a phorbol ester and secretagogues which increase cyclic AMP

1989 ◽  
Vol 67 (10) ◽  
pp. 1321-1325
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Phorbol Ester ◽  
Phosphodiesterase Inhibitor ◽  
Adenosine Monophosphate ◽  
Diabetic Rats ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Streptozotocin Diabetic Rats

We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. We have further studied the effects on growth hormone release from dispersed adenohypophysial cells of normal and streptozotocin diabetic rats of stimulation by compounds that increase cyclic 3′,5′-adenosine monophosphate formation or inhibit its breakdown and of a phorbol ester. The cells of the diabetic rats had no change in sensitivity in response to either cholera toxin or forskolin. A phosphodiesterase inhibitor caused an equal GH release from cells of both diabetic and normal animals after 60 min of incubation. There was no change in sensitivity of the cells of diabetic animals or in the maximal reponse of these cells to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate when compared with normal cells. A low calcium medium that blocked growth hormone releasing factor stimulated growth hormone release from normal rat cells also blocked it from the cells of the diabetic rats. These results suggest that the defect in response of the somatotrophs of diabetic animals is specific and only occurs with the hypothalamic hormones and not with other secretagogues.Key words: growth hormone, diabetes, streptozotocin, cyclic AMP, phorbol ester.

Altered release of growth hormone from dispersed adenohypophysial cells of streptozotocin diabetic rats. I. Effects of growth hormone releasing factor and somatostatin

1989 ◽  
Vol 67 (10) ◽  
pp. 1315-1320 ◽  
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala
Keyword(s):  
Growth Hormone ◽  
Early Morning ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Rat Growth ◽  
Streptozotocin Diabetic Rats

As growth hormone has been implicated in the "dawn phenomenon," an early morning rise in serum glucose, we have studied the control of growth hormone release in diabetes using an acutely dispersed system of adenohypophysial cells from normal or diabetic rats (65 mg/kg streptozotocin, 8 days before sacrifice; serum glucose, 490 ± 17 mg/dL). Growth hormone release is normally controlled by the two hypothalamic hormones, growth hormone releasing factor and somatostatin. We have found cells of the diabetic rats exhibit changes in sensitivity that result in increased growth hormone release in static incubation. In normal cells, rat growth hormone releasing factor increases growth hormone release three- to four-fold with an EC50 of 151 ± 27 pM (n = 7). In contrast, in cells from diabetic rats, there was a significant (twofold) increase in sensitivity to growth hormone releasing factor (EC50 = 75 ± 15 pM, n = 7) which resulted in increased growth hormone release with lower but not maximal (10 nM) growth hormone releasing factor. Basal nonstimulated release was unchanged. Somatostatin inhibition of stimulated growth hormone release was reduced (n = 7); half-maximal inhibition occurred with 0.21 ± 0.03 nM (normal) and 0.76 ± 0.17 nM somatotatin (diabetic). In perifusion the peak secretion rate was significantly lower for diabetic cells stimulated by a maximal dose of growth hormone releasing factor. These studies suggest somatotrophs of diabetic rats have altered sensitivity in vitro to the controlling hormones growth hormone releasing factor and somatostatin.Key words: growth hormone, diabetes, streptozotocin, growth hormone releasing factor, somatostatin.

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