Stimulation by Gastric Inhibitory Polypeptide of Insulin and Glucagon Secretion by Rat Islet Cultures

Wilfred Y. Fujimoto; John W. Ensinck; Frederick W. Merchant; Robert H. Williams; Phillip H. Smith; David G. Johnson

doi:10.3181/00379727-157-39997

Stimulation by Gastric Inhibitory Polypeptide of Insulin and Glucagon Secretion by Rat Islet Cultures

Wilfred Y. Fujimoto, John W. Ensinck, Frederick W. Merchant, Robert H. Williams, Phillip H. Smith, David G. Johnson

Medicine

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

Physiologic amounts of GIP stimulated the secretion of IRI and IRG by monolayer cultures of neonatal rat pancreatic islets. Localization of exogenous GIP to a minority subpopulation of the islet cells was observed. The results may be interpreted to indicate that the effect of GIP on IRI release by the B cell is not direct, but rather, is mediated through its action on another islet cell type. Conversely, the action of GIP on IRG release may be directly mediated through an effect of GIP on the A cell. The action of GIP on IRG release apparently overrides any sup pressive effect that high glucose levels may exert. The stimulation by GIP of both IRI and IRG release was greater when a mixture of amino acids was omitted.

Original language	English (US)
Pages (from-to)	89-93
Number of pages	5
Journal	Proceedings of the Society for Experimental Biology and Medicine
Volume	157
Issue number	1
DOIs	https://doi.org/10.3181/00379727-157-39997
State	Published - Jan 1978

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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title = "Stimulation by Gastric Inhibitory Polypeptide of Insulin and Glucagon Secretion by Rat Islet Cultures",

abstract = "Physiologic amounts of GIP stimulated the secretion of IRI and IRG by monolayer cultures of neonatal rat pancreatic islets. Localization of exogenous GIP to a minority subpopulation of the islet cells was observed. The results may be interpreted to indicate that the effect of GIP on IRI release by the B cell is not direct, but rather, is mediated through its action on another islet cell type. Conversely, the action of GIP on IRG release may be directly mediated through an effect of GIP on the A cell. The action of GIP on IRG release apparently overrides any sup pressive effect that high glucose levels may exert. The stimulation by GIP of both IRI and IRG release was greater when a mixture of amino acids was omitted.",

author = "Fujimoto, {Wilfred Y.} and Ensinck, {John W.} and Merchant, {Frederick W.} and Williams, {Robert H.} and Smith, {Phillip H.} and Johnson, {David G.}",

note = "Funding Information: Supported in part by USPHS Grants AM02456, AM15312, AM16008, and AM17698, by the Kroc Foundation, by the Diabetes-Endocrinology Research Center (AM17047), and by the Washington Diabetes Association. Drs. Fujimoto and Johnson were recipients of Research Career Development Awards AM47142 and AM70727, respectively. Address reprint requests to Dr. Fujimoto at the Department of Medicine, RG-20, University of Washington, Seattle, Washington 98195. 1 1978 157 1 89 93 ",

year = "1978",

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doi = "10.3181/00379727-157-39997",

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AU - Fujimoto, Wilfred Y.

AU - Ensinck, John W.

AU - Merchant, Frederick W.

AU - Williams, Robert H.

AU - Smith, Phillip H.

AU - Johnson, David G.

N1 - Funding Information: Supported in part by USPHS Grants AM02456, AM15312, AM16008, and AM17698, by the Kroc Foundation, by the Diabetes-Endocrinology Research Center (AM17047), and by the Washington Diabetes Association. Drs. Fujimoto and Johnson were recipients of Research Career Development Awards AM47142 and AM70727, respectively. Address reprint requests to Dr. Fujimoto at the Department of Medicine, RG-20, University of Washington, Seattle, Washington 98195. 1 1978 157 1 89 93

PY - 1978/1

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N2 - Physiologic amounts of GIP stimulated the secretion of IRI and IRG by monolayer cultures of neonatal rat pancreatic islets. Localization of exogenous GIP to a minority subpopulation of the islet cells was observed. The results may be interpreted to indicate that the effect of GIP on IRI release by the B cell is not direct, but rather, is mediated through its action on another islet cell type. Conversely, the action of GIP on IRG release may be directly mediated through an effect of GIP on the A cell. The action of GIP on IRG release apparently overrides any sup pressive effect that high glucose levels may exert. The stimulation by GIP of both IRI and IRG release was greater when a mixture of amino acids was omitted.

AB - Physiologic amounts of GIP stimulated the secretion of IRI and IRG by monolayer cultures of neonatal rat pancreatic islets. Localization of exogenous GIP to a minority subpopulation of the islet cells was observed. The results may be interpreted to indicate that the effect of GIP on IRI release by the B cell is not direct, but rather, is mediated through its action on another islet cell type. Conversely, the action of GIP on IRG release may be directly mediated through an effect of GIP on the A cell. The action of GIP on IRG release apparently overrides any sup pressive effect that high glucose levels may exert. The stimulation by GIP of both IRI and IRG release was greater when a mixture of amino acids was omitted.

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Stimulation by Gastric Inhibitory Polypeptide of Insulin and Glucagon Secretion by Rat Islet Cultures

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