scholarly journals Effect of a non-sulphonylurea hypoglycaemic agent, KAD-1229 on hormone secretion in the isolated perfused pancreas of the rat

1996 ◽  
Vol 117 (8) ◽  
pp. 1702-1706 ◽  
Author(s):  
Mayumi Kinukawa ◽  
Hideki Ohnota ◽  
Yukiyoshi Ajisawa
1991 ◽  
Vol 260 (1) ◽  
pp. E59-E66 ◽  
Author(s):  
J. W. Starnes ◽  
E. Cheong ◽  
F. M. Matschinsky

This is the first study investigating hormone secretion by the isolated perfused pancreas of the aged Fischer 344 rat. Nutrient-induced release of insulin, glucagon, and somatostatin in overnight-fasted rats aged 2, 10, 18, 24, and 30 mo was studied. After an equilibration period, the pancreas was perfused for 20 min with buffer A (containing 4.2 mM glucose plus a 3.5 mM mixture of amino acids) then for 20 min with buffer B (containing 8.3 mM glucose and 7.0 mM amino acids). When stimulated by buffer B, the amount of insulin secreted increased (P less than 0.05) from immaturity (2 mo) to adulthood (10-18 mo) because of growth of the organ. From adulthood to very old age an equal amount of insulin was released in all groups during the last 19 min of perfusion with buffer B. Fasting blood glucose levels remained constant throughout life, whereas pancreatic insulin stores and plasma insulin levels rose, reaching peak values at 18 mo. The alpha-cell appeared to be deemphasized relative to the beta-cell during development but not thereafter, as indicated by the findings that from immaturity to adulthood pancreatic glucagon stores expanded less than insulin stores and that glucagon release significantly decreased. Only minor changes in somatostatin release from the delta-cells were observed after the rat reached adulthood. We conclude that the endocrine secretory response of the pancreas is well maintained throughout life in the Fischer 344 rat.


1981 ◽  
Vol 241 (2) ◽  
pp. E146-E150
Author(s):  
S. Seino ◽  
Y. Seino ◽  
J. Takemura ◽  
K. Tsuda ◽  
H. Kuzuya ◽  
...  

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.


Endocrinology ◽  
1985 ◽  
Vol 117 (5) ◽  
pp. 1996-2000 ◽  
Author(s):  
YUKINOBU CHIBA ◽  
KOICHI KAWAI ◽  
YUKICHI OKUDA ◽  
EISUKE MUNEKATA ◽  
KAMEJIRO YAMASHITA

1989 ◽  
Vol 256 (5) ◽  
pp. E619-E623
Author(s):  
T. Yoshimura ◽  
J. Ishizuka ◽  
G. H. Greeley ◽  
J. C. Thompson

We have examined the effect of galanin infusion on glucose-stimulated release of insulin from the isolated perfused pancreas of the rat to better characterize the effect of galanin on the first and second phases of insulin release. The effects of galanin on insulin release stimulated by L-arginine or high concentrations of potassium were also examined. When perfusion of galanin was started 4 min before the start of perfusion of high glucose (16.7 mM), galanin (10(-8)-10(-11) M) inhibited both the first and second phases of insulin release in a dose-dependent manner. When perfusion of galanin (10(-8) or 10(-9) M) was started simultaneously with high glucose (16.7 mM), only the second phase of insulin release was suppressed (P less than 0.05). Galanin (10(-9) M) failed to inhibit insulin release stimulated by L-arginine (10 and 5 mM) or potassium (25 and 20 mM). These findings suggest that the inhibitory action of galanin on glucose-stimulated insulin release is exerted on early intracellular events that occur during the stimulation of insulin release and that are common to both phases. Because galanin does not inhibit insulin release stimulated by L-arginine or potassium, galanin may inhibit glucose-stimulated closure of potassium channels.


1994 ◽  
Vol 86 (3) ◽  
pp. 311-316 ◽  
Author(s):  
Dr Hiroshi Hirose ◽  
Hiroshi Maruyama ◽  
Koichi Kido ◽  
Katsuhiko Ito ◽  
Kazunori Koyama ◽  
...  

1. The effects of various stimuli, including changes in glucose concentration, arginine, tyramine and noradrenaline, on insulin and glucagon secretion were investigated using isolated perfused pancreata of obese and lean male Zucker rats at 12 months of age. 2. In Zucker fatty rats, the insulin secretion rate was significantly (P < 0.01) higher than that of lean rats at all glucose concentrations tested (8.3, 16.7 and 1.4 mmol/l). However, the integrated insulin secretory response to raising the glucose concentration from 8.3 to 16.7 mmol/l was almost absent in these rats. The glucagon secretion rates were significantly lower at 8.3 and 1.4 mmol/l glucose (P < 0.001 for both), and in responses to 10 μg/ml tyramine and 0.1 μmol/l noradrenaline (P < 0.05 for both), in Zucker fatty rats. Integrated insulin and glucagon responses to 10 mmol/l arginine were identical in the two groups. 3. Histopathological and immunochemical studies revealed hyperplasia of β-cells and scattered α-cells in the enlarged islets of Zucker fatty rats. 4. These results suggest that, in Zucker fatty rats, the decreased glucagon secretion in the isolated perfused pancreas is attributable to changes in the environment of α-cells and/or the inhibitory effects of hypersecreted insulin.


Cryobiology ◽  
1984 ◽  
Vol 21 (6) ◽  
pp. 688
Author(s):  
L.-H. Toledo-Pereyra

1989 ◽  
Vol 2 (3) ◽  
pp. 165-167 ◽  
Author(s):  
J. Wahlberg ◽  
J. H. Southard ◽  
F. O. Belzer

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