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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0012984,
umls-concept:C0017687,
umls-concept:C0019932,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205409,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C0702058,
umls-concept:C1280500,
umls-concept:C1283071,
umls-concept:C1549542,
umls-concept:C1707455,
umls-concept:C1963578
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pubmed:issue |
4
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pubmed:dateCreated |
1989-5-3
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pubmed:abstractText |
Recently, it has been demonstrated that glucagon-like peptide-1 (GLP-1)-(7-37) possesses a potent insulinotropic activity. In this paper, we compared the effects of GLP-1-(1-37) and -(7-37) and glucagon on insulin, glucagon, and somatostatin release from isolated perfused canine and rat pancreases under the perfusate condition of 5.5 mM glucose plus arginine. With canine pancreas perfusion, 1 nM GLP-1-(7-37) was more potent in stimulating insulin and somatostatin release than was the same dose of glucagon [stimulation to 375 +/- 36% vs. 302 +/- 28% of the basal level for insulin (P less than 0.05); 724 +/- 129% vs. 311 +/- 33% of the basal level for somatostatin (P less than 0.01)]. GLP-1-(1-37) (1 nM) did not stimulate either insulin or somatostatin release. GLP-1-(7-37) (1 nM) decreased the glucagon level of the effluent perfusate to 67.2 +/- 3.4% of its basal level; but 1 nM GLP-1-(1-37) did not. Glucagon (1 nM) decreased GLP-1-like immunoreactivity to 64.0 +/- 5.2% of its basal level. With rat pancreatic perfusion, the minimal dose for stimulation of insulin release was 100 nM for GLP-1-(1-37), 0.1 nM for GLP-1-(7-37), and 1 nM for glucagon, respectively. Glucagon release was partially inhibited by 100 nM GLP-1-(1-37) and 1 and 10 nM GLP-1-(7-37). The present results indicate that 1) since GLP-1-(7-37) is released from the intestine, it might be an important incretin candidate along with gastric inhibitory peptide; and 2) the release of proglucagon-derived peptides from pancreatic A-cells is regulated by autofeedback through glucagon and GLP-1.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon-Like Peptide 1,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon-Like Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin,
http://linkedlifedata.com/resource/pubmed/chemical/glucagon-like peptide 1 (1-37),
http://linkedlifedata.com/resource/pubmed/chemical/glucagon-like peptide 1 (7-37)
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
124
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1768-73
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2564338-Animals,
pubmed-meshheading:2564338-Cell Separation,
pubmed-meshheading:2564338-Dogs,
pubmed-meshheading:2564338-Dose-Response Relationship, Drug,
pubmed-meshheading:2564338-Glucagon,
pubmed-meshheading:2564338-Glucagon-Like Peptide 1,
pubmed-meshheading:2564338-Glucagon-Like Peptides,
pubmed-meshheading:2564338-Insulin,
pubmed-meshheading:2564338-Islets of Langerhans,
pubmed-meshheading:2564338-Male,
pubmed-meshheading:2564338-Pancreas,
pubmed-meshheading:2564338-Peptide Fragments,
pubmed-meshheading:2564338-Peptides,
pubmed-meshheading:2564338-Perfusion,
pubmed-meshheading:2564338-Rats,
pubmed-meshheading:2564338-Rats, Inbred Strains,
pubmed-meshheading:2564338-Somatostatin
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pubmed:year |
1989
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pubmed:articleTitle |
Comparison of the effects of glucagon-like peptide-1-(1-37) and -(7-37) and glucagon on islet hormone release from isolated perfused canine and rat pancreases.
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pubmed:affiliation |
Department of Internal Medicine, University of Tsukuba, Ibaraki-ken, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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