Somatomedin inhibitors in serum and liver of growth hormone-deficient diabetic rats

Diabetes ◽  
1983 ◽  
Vol 32 (3) ◽  
pp. 262-264 ◽  
Author(s):  
R. Vassilopoulou-Sellin ◽  
C. O. Oyedeji ◽  
N. A. Samaan
Keyword(s):  
Growth Hormone ◽  
Diabetic Rats ◽  
Somatomedin Inhibitors

Somatomedin Inhibitors in Serum and Liver of Growth Hormone-Deficient Diabetic Rats

Diabetes ◽  
1983 ◽  
Vol 32 (3) ◽  
pp. 262-264 ◽  
Author(s):  
R. Vassilopoulou-Sellin ◽  
C. O. Oyedeji ◽  
N. A. Samaan
Keyword(s):  
Growth Hormone ◽  
Diabetic Rats ◽  
Somatomedin Inhibitors

Effects of refeeding of undernourished and insulin treatment of diabetic neonatal rats on IGF and IGFBP

1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Growth Factor ◽  
Mrna Expression ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Insulin Like Growth Factor ◽  
Neonatal Rats ◽  
Igf I ◽  
Serum Gh

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.

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.

scholarly journals Evaluation of the rate-limiting steps in the pathway of glucose metabolism in kidney cortex of normal, diabetic, cortisone-treated and growth hormone-treated rats

1972 ◽  
Vol 128 (5) ◽  
pp. 1293-1301 ◽  
Author(s):  
P. K. Joseph ◽  
K. Subrahmanyam
Keyword(s):  
Amino Acids ◽  
Growth Hormone ◽  
Aspartate Aminotransferase ◽  
Glycogen Content ◽  
Diabetic Rats ◽  
Kidney Cortex ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Ammonia Content ◽  
Citrate Lyase

1. The activities of gluconeogenic and glycolytic enzymes and the concentrations of citrate, ammonia, amino acids, glycogen, glucose 6-phosphate, acetyl-CoA, lactate and pyruvate were measured in kidney cortex of normal, diabetic, cortisone-treated and growth hormone-treated rats. 2. In kidney cortex of diabetic, cortisone-treated and growth hormone-treated rats the activities of glucose 6-phosphatase (EC 3.1.3.9), fructose 1,6-diphosphatase (EC 3.1.3.11) and phosphopyruvate carboxylase (EC 4.1.1.32) were increased. 3. The activities of glutamate dehydrogenase (EC 1.4.1.3), alanine aminotransferase (EC 2.6.1.2), aspartate aminotransferase (EC 2.6.1.10) and pyruvate carboxylase (EC 6.4.1.1) were increased in diabetic and cortisone-treated rats. In growth hormone-treated rats the activity of aspartate aminotransferase was depressed but those of the other three enzymes were unchanged. 4. The activity of hexokinase (EC 2.7.1.1) was not altered in any of these conditions. Phosphofructokinase (EC 2.7.1.11) activity was depressed only in growth hormone-treated rats. Pyruvate kinase (EC 2.7.1.40) activity was depressed in cortisone-treated and growth hormone-treated rats but unchanged in diabetic rats. 5. Amino acids, acetyl-CoA and glucose 6-phosphate contents were increased in rat kidneys in all these three conditions. Ammonia content was increased in diabetic and cortisone-treated rats but was markedly diminished in growth hormone-treated rats. 6. The [lactate]/[pyruvate] ratio was elevated in diabetic and cortisone-treated rats but unchanged in growth hormone-treated rats. Citrate content was increased in the kidney cortex of diabetic and growth hormone-treated rats but was unchanged in cortisone-treated rats. The activity of ATP citrate lyase (EC 4.1.3.8) was depressed in diabetic and growth hormone-treated rats but was increased in cortisone-treated rats. 7. Glycogen content was moderately elevated in growth hormone-treated rats and markedly elevated in diabetic rats, whereas no change in glycogen content was observed in cortisone-treated rats. Glycogen synthetase (EC 2.4.1.11) activity was unchanged in all these three conditions. Phosphorylase (EC 2.4.1.1) activity was not affected in cortisone-treated rats but was depressed in diabetic and growth hormone-treated rats.

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