A biodegradable copolymer for the slow release of growth hormone expedites scarring in diabetic rats

2007 ◽  
Vol 81B (2) ◽  
pp. 291-304 ◽  
Author(s):  
Francisco García-Esteo ◽  
Gemma Pascual ◽  
Alberto Gallardo ◽  
Julio San-Román ◽  
Julia Buján ◽  
...  
Diabetes ◽  
1983 ◽  
Vol 32 (3) ◽  
pp. 262-264 ◽  
Author(s):  
R. Vassilopoulou-Sellin ◽  
C. O. Oyedeji ◽  
N. A. Samaan

Diabetes ◽  
1983 ◽  
Vol 32 (5) ◽  
pp. 478-481 ◽  
Author(s):  
M. F. Goosen ◽  
Y. F. Leung ◽  
G. M. O'Shea ◽  
S. Chou ◽  
A. M. Sun
Keyword(s):  

1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  

The effect of refeeding and insulin treatment of undernourished and diabetic neonatal rats, respectively, on the regulation of insulin-like growth factor (IGF) and insulin-like growth factor binding protein (IGFBP) was investigated. The changes in body weight, insulinemia, glycemia, serum IGF-I, and growth hormone (GH) as well as the increase of the 30-kDa IGFBP in undernourished and diabetic neonatal rats previously shown elsewhere were reversed by refeeding and insulin treatment, respectively. Also, changes in liver mRNA expression of IGF-I and-II and IGFBP-1 and -2 were restored in refed undernourished and IGF-I and IGFBP-1 levels recovered in insulin-treated diabetic rats. However, serum GH was still below normal after rehabilitation in both situations. Thus the present results support the idea of a GH-independent IGF/ IGFBP regulation mediated by a balance of insulin and nutrients as has already been suggested in previous neonatal studies.


Diabetes ◽  
1983 ◽  
Vol 32 (5) ◽  
pp. 478-481 ◽  
Author(s):  
M. F. A. Goosen ◽  
Y. F. Leung ◽  
G. M. O'Shea ◽  
S. Chou ◽  
A. M. Sun

1989 ◽  
Vol 67 (10) ◽  
pp. 1321-1325
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala

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.


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