scholarly journals The Essential Amino Acid Domains in Salivary Peptide P-C That Potentiate Glucose-Induced Insulin Release and Inhibit Arginine-Induced Glucagon Release from Perfused Rat Pancreas

1995 ◽  
Vol 67 (1) ◽  
pp. 79-82 ◽  
Author(s):  
Masayasu Kimura ◽  
Noboru Nakashima ◽  
Ikuko Kimura
Keyword(s):  
Amino Acid ◽  
Insulin Release ◽  
Essential Amino Acid ◽  
Glucagon Release ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Salivary Peptide

scholarly journals Glucose Modulation of Amino Acid-Induced Glucagon and Insulin Release in the Isolated Perfused Rat Pancreas

1974 ◽  
Vol 54 (4) ◽  
pp. 819-832 ◽  
Author(s):  
Anthony S. Pagliara ◽  
Susan N. Stillings ◽  
Barbara Hover ◽  
Duane M. Martin ◽  
Franz M. Matschinsky
Keyword(s):  
Amino Acid ◽  
Insulin Release ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Isolated Perfused Rat Pancreas ◽  
Glucagon And Insulin

Stimulatory effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on insulin and glucagon release from the isolated perfused rat pancreas

1993 ◽  
Vol 129 (5) ◽  
pp. 473-479 ◽  
Author(s):  
Chizuko Yokota ◽  
Koichi Kawai ◽  
Shinichi Ohashi ◽  
Yasuko Watanabe ◽  
Seiji Suzuki ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Dependent Manner ◽  
Glucagon Release ◽  
Perfused Rat Pancreas ◽  
Pancreas Perfusion ◽  
Rat Pancreas ◽  
Pituitary Adenylate Cyclase ◽  
Stimulation Of

Rat pancreas perfusion was performed to study the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on pancreatic hormone release. Under the perfusate glucose concentration of 5.5 mmol/l, 0.1 nmol/l PACAP27 significantly stimulated both insulin and glucagon release. The degree of stimulation was in a dose dependent manner. The stimulation of insulin release was clearly dependent on the perfusate glucose concentration, when compared with 2.8, 5.5 and 8.3 mmol/l. The potency of PACAP38 on the stimulation of insulin release was greater than that of PACAP27 at 5.5 mmol/l of perfusate glucose concentration, but not at 8.3 mmol/l. No differences for glucagon and cAMP release were found between the two peptides. PACAP's stimulatory effects on insulin and glucagon release were completely abolished by an equimolar and ten times lower concentration of somatostatin, respectively. The physiologic significance of these potent effects of PACAP's islet hormones release must be clarified by further studies.

Alpha-2 adrenergic agonism stimulates islet glucagon release from perfused rat pancreas: possible involvement of alpha-2A adrenergic receptor subtype

1992 ◽  
Vol 127 (3) ◽  
pp. 279-283 ◽  
Author(s):  
Hiroshi Hirose ◽  
Hiroshi Maruyama ◽  
Katsuhiko Itoh ◽  
Kazunori Koyama ◽  
Koichi Kido ◽  
...  
Keyword(s):  
Insulin Release ◽  
Adrenergic Receptor ◽  
Receptor Subtype ◽  
Glucagon Release ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Selective Antagonist ◽  
Alpha Adrenoceptor ◽  
Selective Agonists ◽  
Subtype Selective

Although insulin release is known to be inhibited by alpha-2 adrenergic agonism, the effect of alpha adrenergic agonism on islet glucagon release remains controversial. Alpha-2 adrenoceptors are subdivided into alpha-2A and alpha-2B subtypes using receptor binding methods or cloning methodology. This study was designed to confirm the involvement of the alpha-2 adrenoceptor and its subtypes in glucagon release from the isolated, perfused rat pancreas. Both the alpha-2A preferential agonist oxymetazoline and the non-subtype-selective alpha-2 agonist clonidine induced concentration-dependent stimulation of glucagon release, starting at 10−8 and 10−7 mol/l, respectively (p<0.01). In contrast, neither of the two alpha-1 selective agonists, methoxamine and phenylephrine, at concentrations up to 10−6 mol/l affected glucagon release. Furthermore, the non-subtype-selective alpha-2 antagonist rauwolscine at concentrations of 10−6 and 10−5 mol/l and the alpha-1 and alpha-2A selective antagonist WB-4101 at 10−5 mol/l showed significant antagonism of 10−7 mol/l clonidine-induced glucagon release versus corresponding controls. Neither the alpha-1 and alpha-2B selective antagonist prazosin nor the alpha-2B preferential antagonist chlorpromazine, at concentrations up to 10−5 mol/l, antagonized the effects of clonidine. None of the eight drugs, at the concentrations tested, affected insulin release with 5.5 mmol/l glucose. These results suggest that in rats islet glucagon release induced by alpha adrenoceptor agonism is mediated through alpha-2 adrenoceptors, possibly the alpha-2A subtype.

STUDIES ON THE MECHANISM OF SOMATOSTATIN ACTION ON INSULIN RELEASE

1976 ◽  
Vol 81 (4) ◽  
pp. 753-761 ◽  
Author(s):  
S. Efendić ◽  
A. Claro ◽  
R. Luft
Keyword(s):  
Insulin Release ◽  
Basal Insulin ◽  
Potent Inhibitor ◽  
Glucagon Release ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas

ABSTRACT In man, 3 μg per kg per 90 min of linear somatostatin significantly inhibited basal as well as arginine induced insulin and glucagon release. One μg per kg per 90 min of somatostatin significantly inhibited basal insulin release but not basal glucagon release or arginine induced insulin and glucagon release. In the perfused rat pancreas, as little as one ng per ml of perfusate of somatostatin significantly inhibited arginine induced insulin but not glucagon release, while 10 ng per ml of somatostatin by more than 50 per cent reduced the effect of arginine on insulin and glucagon release. Thus, linear somatostatin seemed to be a slightly more potent inhibitor of insulin than of glucagon release in man and in the perfused rat pancreas.

Insulin, glucagon and somatostatin in the perfused rat pancreas and the effects of HB 699 (4-(2-(5-chloro-2 metoxy-benzamido)-ethyl)-benzoic acid)

1981 ◽  
Vol 98 (4) ◽  
pp. 573-579 ◽  
Author(s):  
Suad Efendić ◽  
Franz Enzmann ◽  
Mark Gutniak ◽  
Anita Nylén ◽  
Manfred Zoltobrocki
Keyword(s):  
Benzoic Acid ◽  
Insulin Release ◽  
Basal Insulin ◽  
Glucagon Secretion ◽  
Inhibitory Effect ◽  
Glucagon Release ◽  
Stimulatory Action ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas

Abstract. HB 699 (100 μg/ml), almost identical with the left residue of the sulphonylurea glibenclamide, enhanced basal insulin and somatostatin release from the perfused rat pancreas. The compound also augmented both the early and the late insulin release stimulated by 6.7 mm glucose, while with 16.7 and 33.3 mm glucose only late insulin release was increased. Furthermore, HB699 enhanced both phases of glucose induced somatostatin release irrespective of whether 6.7, 16.7 or 33.3 mM glucose were used. As for glucagon release, HB 699 suppressed basal and arginine stimulated glucagon secretion. The present findings imply that the sulphonylurea moiety of glibenclamide is not a prerequisite for its stimulatory action on insulin and somatostatin release. It is suggested that the enhanced somatostatin release mediates the inhibitory effect of the compound on glucagon release.

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