Inhibition of glucose-stimulated insulin release in the perfused rat pancreas by parathyroid secretory protein-I (Chromogranin-A)

George H. Greeley; James C. Thompson; Jin Ishizuka; Cary W. Cooper; Michael A. Levine; Sven U. Gorr; David V. Cohn

doi:10.1210/endo-124-3-1235

Inhibition of glucose-stimulated insulin release in the perfused rat pancreas by parathyroid secretory protein-I (Chromogranin-A)

George H. Greeley, James C. Thompson, Jin Ishizuka, Cary W. Cooper, Michael A. Levine, Sven U. Gorr, David V. Cohn

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Abstract

The effect of graded doses (10^-10-10^-8M) of highly purified bovine parathyroid secretory protein-I (SP-I; chromogranin-A) or synthetic porcine pancreastatin on glucosestimulated insulin release in the perfused rat pancreas was examined. SP-I (10^-9 M) inhibited the first phase of glucosestimulated insulin release, and 10^-8 M SP-I inhibited both the first and second phases of glucose-stimulated insulin release; 10^-10 M SP-I was inactive. In comparison, pancreastatin at 10^-10 M inhibited the first phase of insulin release, and at 10^-9 and 10^-9 M, pancreastatin inhibited both phases of insulin release. the inhibition by SP-I was achieved at concentrations that normally exist in the general circulation of man. These and other data suggest that circulating SP-I plays a physiological role in the regulation of insulin secretion.

Original language	English (US)
Pages (from-to)	1235-1238
Number of pages	4
Journal	Endocrinology
Volume	124
Issue number	3
DOIs	https://doi.org/10.1210/endo-124-3-1235
State	Published - Mar 1989

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Endocrinology

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title = "Inhibition of glucose-stimulated insulin release in the perfused rat pancreas by parathyroid secretory protein-I (Chromogranin-A)",

abstract = "The effect of graded doses (10-10-10-8M) of highly purified bovine parathyroid secretory protein-I (SP-I; chromogranin-A) or synthetic porcine pancreastatin on glucosestimulated insulin release in the perfused rat pancreas was examined. SP-I (10-9 M) inhibited the first phase of glucosestimulated insulin release, and 10-8 M SP-I inhibited both the first and second phases of glucose-stimulated insulin release; 10-10 M SP-I was inactive. In comparison, pancreastatin at 10-10 M inhibited the first phase of insulin release, and at 10-9 and 10-9 M, pancreastatin inhibited both phases of insulin release. the inhibition by SP-I was achieved at concentrations that normally exist in the general circulation of man. These and other data suggest that circulating SP-I plays a physiological role in the regulation of insulin secretion.",

author = "Greeley, {George H.} and Thompson, {James C.} and Jin Ishizuka and Cooper, {Cary W.} and Levine, {Michael A.} and Gorr, {Sven U.} and Cohn, {David V.}",

year = "1989",

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AU - Greeley, George H.

AU - Thompson, James C.

AU - Ishizuka, Jin

AU - Cooper, Cary W.

AU - Levine, Michael A.

AU - Gorr, Sven U.

AU - Cohn, David V.

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N2 - The effect of graded doses (10-10-10-8M) of highly purified bovine parathyroid secretory protein-I (SP-I; chromogranin-A) or synthetic porcine pancreastatin on glucosestimulated insulin release in the perfused rat pancreas was examined. SP-I (10-9 M) inhibited the first phase of glucosestimulated insulin release, and 10-8 M SP-I inhibited both the first and second phases of glucose-stimulated insulin release; 10-10 M SP-I was inactive. In comparison, pancreastatin at 10-10 M inhibited the first phase of insulin release, and at 10-9 and 10-9 M, pancreastatin inhibited both phases of insulin release. the inhibition by SP-I was achieved at concentrations that normally exist in the general circulation of man. These and other data suggest that circulating SP-I plays a physiological role in the regulation of insulin secretion.

AB - The effect of graded doses (10-10-10-8M) of highly purified bovine parathyroid secretory protein-I (SP-I; chromogranin-A) or synthetic porcine pancreastatin on glucosestimulated insulin release in the perfused rat pancreas was examined. SP-I (10-9 M) inhibited the first phase of glucosestimulated insulin release, and 10-8 M SP-I inhibited both the first and second phases of glucose-stimulated insulin release; 10-10 M SP-I was inactive. In comparison, pancreastatin at 10-10 M inhibited the first phase of insulin release, and at 10-9 and 10-9 M, pancreastatin inhibited both phases of insulin release. the inhibition by SP-I was achieved at concentrations that normally exist in the general circulation of man. These and other data suggest that circulating SP-I plays a physiological role in the regulation of insulin secretion.

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Inhibition of glucose-stimulated insulin release in the perfused rat pancreas by parathyroid secretory protein-I (Chromogranin-A)

Abstract

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