Truncated glucagon-like peptide−1 and oxyntomodulin stimulate somatostatin release from rabbit fundic D-cells in primary culture
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چکیده
منابع مشابه
Glycine-extended gastrin enhances somatostatin release from cultured rabbit fundic D-cells
The role of the peptide hormone gastrin in stimulating gastric acid secretion is well established. Mature amidated gastrin is processed from larger peptide precursor forms. Increasingly these processing intermediates, such as glycine-extended gastrin (G-Gly) and progastrin, have been shown to have biological activities of their own, often separate and complementary to gastrin. Although G-Gly is...
متن کاملMechanisms for muscarinic inhibition of somatostatin release from canine fundic D cells.
We undertook the present studies to explore the mechanisms by which carbachol inhibits the release of somatostatin-like immunoreactivity (SLI) from D cells. D cells were isolated from canine fundic mucosa by collagenase/EDTA dispersion followed by counterflow elutriation. Carbachol inhibited the release of SLI induced by forskolin, dibutyryl 3':5' cyclic adenosine monophosphate (cAMP), pentagas...
متن کاملBiosynthesis of somatostatin in canine fundic D cells.
The observation that virtually all of the somatostatin-like immunoreactivity in the stomach consists of somatostatin-14 (S14), to the exclusion of somatostatin-28 (S28), suggests a unique pattern of prosomatostatin posttranslational processing. In order to examine the mechanisms by which S14 is produced from its precursor in the stomach, we investigated the biosynthesis of somatostatin in isola...
متن کاملThe histamine H3 receptor agonist N-methylhistamine produced by Helicobacter pylori does not alter somatostatin release from cultured rabbit fundic D-cells
Background—The mechanisms underlying the suppression of somatostatin dependent reflexes in Helicobacter pylori infection are not fully determined. The H pylori product N-methylhistamine and inflammatory mediators such as tumour necrosis factor-á (TNF-á) may be responsible for the alterations in somatostatin release. Aims—To examine the eVect of N-methylhistamine on somatostatin release from cul...
متن کاملThe histamine H3 receptor agonist N alpha-methylhistamine produced by Helicobacter pylori does not alter somatostatin release from cultured rabbit fundic D-cells.
BACKGROUND The mechanisms underlying the suppression of somatostatin dependent reflexes in Helicobacter pylori infection are not fully determined. The H pylori product N alpha-methylhistamine and inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha) may be responsible for the alterations in somatostatin release. AIMS To examine the effect of N alpha-methylhistamine on somato...
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ژورنال
عنوان ژورنال: Experimental Physiology
سال: 1996
ISSN: 0958-0670
DOI: 10.1113/expphysiol.1996.sp003988