Effects of PHI on hormonal secretion from perfused rat pancreas

1983 ◽  
Vol 245 (4) ◽  
pp. E313-E317
Author(s):  
J. Szecowka ◽  
D. Tendler ◽  
S. Efendic

Effects of the novel gastrointestinal polypeptide PHI with N-terminal histidine, C-terminal isoleucine amide, and 27 amino acids have been studied in isolated perfused rat pancreas. PHI increased the release of insulin, glucagon, and somatostatin. The amounts of these hormones released were strictly dependent on the prevailing glucose concentrations. In the absence of glucose, PHI (1 nmol/liter) stimulated glucagon release. In the presence of 4.4 and 6.7 mmol/liter glucose, the same dose of this peptide stimulated insulin and somatostatin release. In the presence of 16.7 mmol/liter glucose, only insulin secretion was increased by PHI. When arginine was used as a secretagogue, PHI (10 nmol/liter) potentiated secretion of insulin, glucagon, and somatostatin. Thus, PHI may take part in the regulation of the function of the pancreatic A, B, and D cells.

Endocrinology ◽  
1984 ◽  
Vol 114 (4) ◽  
pp. 1086-1089 ◽  
Author(s):  
GEGHAM BARSEGHIAN ◽  
CYNTHIA TOMKINSON ◽  
DAVID L. HWANG ◽  
ARYE LEV-RAN

Endocrinology ◽  
1978 ◽  
Vol 102 (5) ◽  
pp. 1496-1500 ◽  
Author(s):  
YASUO GOTO ◽  
YUTAKA SEINO ◽  
TOMOHIKO TAMINATO ◽  
YOSHIMICHI INOUE ◽  
SEIZO KADOWAKI ◽  
...  

1984 ◽  
Vol 105 (4) ◽  
pp. 534-538 ◽  
Author(s):  
P. P. G. Gerber ◽  
E. R. Trimble ◽  
L. Herberg ◽  
A. E. Renold

Abstract. The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. As expected, when the pancreases of non-diabetic rats were exposed to 16.7 mM glucose on two occasions, 20 min apart, insulin secretion during the second period of exposure to high glucose was greater than that during the first period. By contrast, there was no potentiation of somatostatin secretion during the second glucose stimulation with respect to that of the first. Indeed, when the basal glucose concentration was low (1.4 or 2.8 mm) somatostatin secretion during the second glucose stimulation was lower than that during the first. Since exogenous insulin is known to inhibit glucoseinduced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucosestimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. In addition, the absence of potentiated somatostatin secretion could not be attributed to partial inhibition of the D cell by insulin.


1975 ◽  
Vol 117 (1) ◽  
pp. 79-83 ◽  
Author(s):  
TAKAYOSHI TOYOTA ◽  
KANJI ABE ◽  
MIKIHIKO KUDO ◽  
KENICHI KIMURA ◽  
YOSHIO GOTO

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