Oxyntomodulin and related peptides control somatostatin secretion in RIN T3 cells
We studied the effects of oxyntomodulin (OXM), of its C-terminal (19–37) fragment (OXM (19–37)) and of glucagon (GLU) on somatostatin release, cyclic AMP accumulation and inositol phosphate turnover in somatostatin-secreting RIN T3 cells in culture. Rapid changes in cellular free Ca 2+ were also mea...
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Published in | Biochimica et biophysica acta Vol. 1095; no. 3; pp. 249 - 254 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier B.V
12.11.1991
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | We studied the effects of oxyntomodulin (OXM), of its C-terminal (19–37) fragment (OXM (19–37)) and of glucagon (GLU) on somatostatin release, cyclic AMP accumulation and inositol phosphate turnover in somatostatin-secreting RIN T3 cells in culture. Rapid changes in cellular free Ca
2+ were also measured using fura-2. Carbachol was used as a control test agent for the parameters involving the inositol phosphate/Ca
2+ cascade. OXM, GLU and OXM (19–37) were all able to stimulate somatostatin release with relative ED
50 of approx. 1, 22 and 45, respectively. OXM and GLU stimulated cyclic AMP levels with relative ED
50 of approx. 1 and 30, respectively, whereas OXM (19–37) was totally ineffective on this parameter. In contrast to cariachiol, none of the peptides significantly modified the inositol phosphate turnover or induced rapid changes in cellular free Ca
2+. We conclude that the RIN T3 cells contain a receptor-cyclic AMP system similar to that found in gastric mucosa and that this system is linked to somatostatin release. Another receptor-second messenger mechanism linked to somatostatin release is triggered by the (19–37) fragment. This mechanism is not the inositol phosphate/Ca
2+ cascade triggered in the same cells by cholinergic agents. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0167-4889 0006-3002 1879-2596 |
DOI: | 10.1016/0167-4889(91)90107-9 |