Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents

Jin Ishizuka, Kazuhiko Tatemoto, David V. Cohn, James C. Thompson, George H. Greeley

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and l-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 ± 0.9 ng/8 min; second phase: 34.5 ± 1.6 ng/25 min in controls; 16.5 ± 1.1 ng/8 min and 44.0 ± 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of l-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 ± 0.5 ng/5 min in controls, 8.4 ± 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.

Original languageEnglish (US)
Pages (from-to)25-32
Number of pages8
JournalRegulatory Peptides
Volume34
Issue number1
DOIs
StatePublished - Jun 11 1991

Fingerprint

Chromogranin A
Insulin
Sincalide
Gastric Inhibitory Polypeptide
Glucagon
Arginine
pancreastatin
Rats
Pancreas
B-Lymphocytes
Swine
Tuning
Cells

Keywords

  • CCK-8
  • GIP
  • Glucagon
  • l-Arginine
  • Rat pancreas

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Neuroscience(all)

Cite this

Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents. / Ishizuka, Jin; Tatemoto, Kazuhiko; Cohn, David V.; Thompson, James C.; Greeley, George H.

In: Regulatory Peptides, Vol. 34, No. 1, 11.06.1991, p. 25-32.

Research output: Contribution to journalArticle

Ishizuka, Jin ; Tatemoto, Kazuhiko ; Cohn, David V. ; Thompson, James C. ; Greeley, George H. / Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents. In: Regulatory Peptides. 1991 ; Vol. 34, No. 1. pp. 25-32.
@article{2220afc30e78403ca2fdf570b3735aec,
title = "Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents",
abstract = "The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and l-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 ± 0.9 ng/8 min; second phase: 34.5 ± 1.6 ng/25 min in controls; 16.5 ± 1.1 ng/8 min and 44.0 ± 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of l-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 ± 0.5 ng/5 min in controls, 8.4 ± 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.",
keywords = "CCK-8, GIP, Glucagon, l-Arginine, Rat pancreas",
author = "Jin Ishizuka and Kazuhiko Tatemoto and Cohn, {David V.} and Thompson, {James C.} and Greeley, {George H.}",
year = "1991",
month = "6",
day = "11",
doi = "10.1016/0167-0115(91)90221-2",
language = "English (US)",
volume = "34",
pages = "25--32",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents

AU - Ishizuka, Jin

AU - Tatemoto, Kazuhiko

AU - Cohn, David V.

AU - Thompson, James C.

AU - Greeley, George H.

PY - 1991/6/11

Y1 - 1991/6/11

N2 - The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and l-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 ± 0.9 ng/8 min; second phase: 34.5 ± 1.6 ng/25 min in controls; 16.5 ± 1.1 ng/8 min and 44.0 ± 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of l-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 ± 0.5 ng/5 min in controls, 8.4 ± 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.

AB - The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and l-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 ± 0.9 ng/8 min; second phase: 34.5 ± 1.6 ng/25 min in controls; 16.5 ± 1.1 ng/8 min and 44.0 ± 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of l-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 ± 0.5 ng/5 min in controls, 8.4 ± 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.

KW - CCK-8

KW - GIP

KW - Glucagon

KW - l-Arginine

KW - Rat pancreas

UR - http://www.scopus.com/inward/record.url?scp=0025859288&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025859288&partnerID=8YFLogxK

U2 - 10.1016/0167-0115(91)90221-2

DO - 10.1016/0167-0115(91)90221-2

M3 - Article

C2 - 1857778

AN - SCOPUS:0025859288

VL - 34

SP - 25

EP - 32

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

IS - 1

ER -