1991
DOI: 10.1016/0014-5793(91)80182-3
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Functional receptors for the insulinotropic hormone glucagon‐like peptide‐I(7–37) on a somatostatin secreting cell line

Abstract: Glucagon‐like peptide‐I (7–37) [(GLP‐I(7–37)] is an instestinal peptide hormone that has potent insulinotropic activities in vivo in response to oral nutrients. In the isolated perfused pancreas, and in vitro in cultured B cells, GLP‐I(7–37) receptor binding and GLP‐I(7–37)‐induced cAMP generation and harmone secretion was studied using cell lines producing insulin/B cell (βTC‐1), glucagon/A cell (INR1G9) and somatostatin/D cell (RIN 1027‐B2). [125I]GLP‐I(7–37) bound specifically to both B and D cells but not … Show more

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Cited by 88 publications
(55 citation statements)
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“…The concentration resulting in half-maximal inhibition (IC 50 ) of binding to the human GLP-1 receptor expressed in CHO-K1 cells was 5.5 Ϯ 1.3 nM for GLP-1 (7-36) amide, a value within the range of those reported for GLP-1 binding to the endogenous receptor found in islet cell lines and to the recombinant receptor expressed in COS-7 cells (Goke and Conlon, 1988;Goke et al, 1989;Fehmann and Habener, 1991;Thorens, 1992;Wheeler et al, 1993). The IC 50 value of ZP10A for the human GLP-1 receptor was 1.4 Ϯ 0.2 nM, which was approximately 4 times higher than the affinity of GLP-1 (7-36) amide.…”
Section: Resultssupporting
confidence: 52%
“…The concentration resulting in half-maximal inhibition (IC 50 ) of binding to the human GLP-1 receptor expressed in CHO-K1 cells was 5.5 Ϯ 1.3 nM for GLP-1 (7-36) amide, a value within the range of those reported for GLP-1 binding to the endogenous receptor found in islet cell lines and to the recombinant receptor expressed in COS-7 cells (Goke and Conlon, 1988;Goke et al, 1989;Fehmann and Habener, 1991;Thorens, 1992;Wheeler et al, 1993). The IC 50 value of ZP10A for the human GLP-1 receptor was 1.4 Ϯ 0.2 nM, which was approximately 4 times higher than the affinity of GLP-1 (7-36) amide.…”
Section: Resultssupporting
confidence: 52%
“…Current concepts of GLP-1R-dependent inhibition of islet ␣-cell secretory activity involve both GLP-1R-dependent stimulation of the ␤-or ␦-cell (26,27) liberating indirect mediators, such as insulin or somatostatin, as well as the direct inhibitory action of GLP-1 itself directly on the ␣-cell (28). The finding that Ex-4 failed to decrease levels of plasma glucagon in ␤-cell Pdx1Ϫ/Ϫ mice, taken together with the defect observed in GLP-1R-dependent insulin secretion, strongly implicates a fully functional ␤-cell as a critical Data show the gene expression profile in ␤-cell Pdx1Ϫ/Ϫ islets (pool of 15 islets) incubated in RPMI-1640 media with 11 mmol/l glucose for 24 h (n ϭ 6 for ␤-cell Pdx1ϩ/ϩ islets and n ϭ 4 for ␤-cell Pdx1Ϫ/Ϫ islets).…”
Section: Discussionmentioning
confidence: 99%
“…It is conceivable that the GLP-I inhibition of glucagon release, an effect that is of therapeutical value in NIDDM, is mediated via the paracrine effects of GLP-I-stimulated insulin release. Alternatively, since GLP-I receptors are present on a somatostatin-secreting cell line (30), paracrine effects including somatostatininhibited glucagon release (20) can be involved. Fourth, the reported in vivo stimulation of glucagon release by GIP observed in the perfused pancreas in the presence of low glucose concentrations (31,32) seems attributable to direct interactions of this peptide with pancreatic a-cells.…”
Section: Discussionmentioning
confidence: 99%