In vitro motor activity and compliance of the caecum in streptozotocin diabetic rats.

1990 ◽  
Vol 40 (6) ◽  
pp. 843-851 ◽  
Author(s):  
Hua Sheng LIU ◽  
Takeo KARAKIDA ◽  
Shinji HOMMA
Keyword(s):  
Motor Activity ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

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.

Satellite cells derived from streptozotocin-diabetic rats display altered fusion parameters in vitro

Metabolism ◽  
1989 ◽  
Vol 38 (4) ◽  
pp. 348-352 ◽  
Author(s):  
M.A. Brannon ◽  
M.V. Dodson ◽  
B.A. Wheeler ◽  
B.D. Mathison ◽  
B.A. Mathison
Keyword(s):  
Satellite Cells ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

scholarly journals Enhanced proteolytic activity directed against the N-terminal of IGF-I in diabetic rats

1999 ◽  
Vol 162 (2) ◽  
pp. 243-250 ◽  
Author(s):  
H Yamamoto ◽  
C Maake ◽  
LJ Murphy
Keyword(s):  
Protease Activity ◽  
Insulin Treatment ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Acute Administration ◽  
Mrna Levels ◽  
Igf I ◽  
Streptozotocin Diabetic Rats ◽  
Biotin Label

We have recently identified in serum an acid protease which is capable of generating des(1-3)IGF-I from intact IGF-I. Here we have utilized a synthetic substrate with the sequence, biotin-G-P-E-T-L-C-BSA which contains the N-terminal sequence of IGF-I, to investigate the levels of this protease activity in streptozotocin-diabetic rats. Protease activity, quantified in terms of the amount of the biotin label lost, was determined in serum and hepatic extracts from normal control rats, diabetic rats and insulin-treated diabetic rats. Both the serum protease activity and protease activity in hepatic extracts were significantly increased in diabetic rats compared with control rats (P<0.02 and P<0.005). Following acute administration of insulin, a rapid and marked reduction in serum protease activity was observed; with an approximately 50% reduction apparent at 30 min (P<0.001). Chronic insulin treatment of diabetic rats also significantly reduced the serum and hepatic protease activity to the levels seen in control rats. A positive correlation between protease activity and serum glucose level was observed (r=0.58, P<0.005). The abundance of Spi 2.1 mRNA, a serine protease inhibitor, capable of inhibiting the IGF-I protease activity in vitro, was significantly decreased in the liver of diabetic rats and insulin treatment of diabetic rats did not normalize Spi 2.1 mRNA levels. These data suggest that the conversion of IGF-I to the more active des(1-3)IGF-I variant may be enhanced in diabetic animals. Since serum IGF-I levels are reduced in diabetic rats, increased des(1-3)IGF-I-generating protease activity would enhance the functional activity of the circulating IGF-I.

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