glucagon-like-peptide-1-(7-36) and inositol-2-monophosphate

glucagon-like-peptide-1-(7-36) has been researched along with inositol-2-monophosphate* in 1 studies

Other Studies

1 other study(ies) available for glucagon-like-peptide-1-(7-36) and inositol-2-monophosphate

ArticleYear
GLP-1-(7-36) amide, -(1-37), and -(1-36) amide: potent cAMP-dependent stimuli of rat parietal cell function.
    The American journal of physiology, 1991, Volume: 260, Issue:6 Pt 1

    We investigated the effect of glucagon-like peptide 1 (GLP-1)-(7-36) amide and its molecular variants GLP-1-(1-37) and GLP-1-(1-36) amide on enzymatically dispersed enriched rat parietal cells using [14C]aminopyrine accumulation as a measure of H+ production. GLP-1-(7-36) amide was 100 times more potent than GLP-1-(1-37) and GLP-1-(1-36) amide in stimulating [14C]aminopyrine accumulation. At their maximally effective concentrations, GLP-1-(7-36) amide (10(-8) M), GLP-1-(1-37) (10(-6) M), and GLP-1-(1-36) amide (10(-6) M) reached 80-90% of the response to 10(-4) M histamine. However, the peptides were 100-10,000 times more potent than histamine, which induced maximal [14C]aminopyrine accumulation at 10(-4) M. Stimulation by GLP-1 was dependent on the presence of a phosphodiesterase inhibitor and was not altered by pertussis toxin. Ranitidine failed to affect the response to the GLP-1 variants. Stimulation of H+ production by GLP-1 was accompanied by an increase in the formation of adenosine 3',5'-cyclic monophosphate (cAMP) but not by changes in phosphoinositol breakdown. In stimulating [14C]aminopyrine accumulation, the GLP-1 variants acted additively to threshold but not to maximal concentrations of histamine, suggesting that histamine and GLP-1 activate the same cAMP pool. In contrast, in anesthetized rats GLP-1-(7-36) amide (10-500 ng.kg-1.h-1) had no effect on basal and pentagastrin-stimulated acid secretion in vivo. We conclude that GLP-1 exerts a direct stimulatory effect on rat parietal cells. This potent effect is mediated by cAMP and is independent of H2 receptors. In vivo direct stimulation by GLP-1 of the parietal cells might be counterbalanced by indirect inhibitory mechanisms that are excluded in the in vitro cell system.

    Topics: 1-Methyl-3-isobutylxanthine; Aminopyrine; Animals; Biological Transport; Bucladesine; Carbachol; Colforsin; Cyclic AMP; Female; Gastric Acid; Glucagon; Glucagon-Like Peptide 1; Glucagon-Like Peptides; Histamine; In Vitro Techniques; Inositol Phosphates; Kinetics; Parietal Cells, Gastric; Peptide Fragments; Peptides; Pertussis Toxin; Rats; Rats, Inbred Strains; Virulence Factors, Bordetella

1991