INT18400

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Context Info
Confidence 0.80
First Reported 1984
Last Reported 2011
Negated 2
Speculated 1
Reported most in Abstract
Documents 97
Total Number 98
Disease Relevance 11.96
Pain Relevance 24.32

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

plasma membrane (Glp1r) signal transducer activity (Glp1r)
Anatomy Link Frequency
ileum 8
gut 5
intestinal epithelium 3
intestine 3
endocrine cells 2
Glp1r (Rattus norvegicus)
Pain Link Frequency Relevance Heat
tolerance 167 100.00 Very High Very High Very High
agonist 140 100.00 Very High Very High Very High
Somatostatin 81 100.00 Very High Very High Very High
qutenza 51 100.00 Very High Very High Very High
Central nervous system 306 99.98 Very High Very High Very High
Cholecystokinin 20 99.96 Very High Very High Very High
narcan 2 99.92 Very High Very High Very High
Neurotransmitter 70 99.84 Very High Very High Very High
substance P 48 99.82 Very High Very High Very High
Neuropeptide 54 99.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
Aids-related Complex 477 100.00 Very High Very High Very High
Impaired Glucose Tolerance 169 100.00 Very High Very High Very High
Diabetes Mellitus 437 99.72 Very High Very High Very High
Pancreatitis 256 99.38 Very High Very High Very High
Myocardial Infarction 106 95.76 Very High Very High Very High
Gastric Motility Disorder 5 95.68 Very High Very High Very High
Rheumatoid Arthritis 18 92.28 High High
Hyperglycemia 42 91.76 High High
Hyperlipidemia 25 91.52 High High
Hyperinsulinism 31 88.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Glucagon-like peptide-1 (GLP-1) is released after food intake to act as an incretin.
Localization (released) of Glucagon-like peptide-1
1) Confidence 0.80 Published 2008 Journal Neurogastroenterol. Motil. Section Abstract Doc Link 18298441 Disease Relevance 0.15 Pain Relevance 0.29
Glucagon-like peptide-1 (GLP-1) is released after food intake to act as an incretin.
Localization (released) of GLP-1
2) Confidence 0.80 Published 2008 Journal Neurogastroenterol. Motil. Section Abstract Doc Link 18298441 Disease Relevance 0.15 Pain Relevance 0.29
It enhanced GLP-1 release up to sixfold above basal during the early phase followed by a sustained secretion at 400% above basal.
Localization (release) of GLP-1
3) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.33
Paradoxically, GLP-1 originates from the lower intestines and therefore a complex regulation of postprandial GLP-1 secretion must exist.
Localization (secretion) of GLP-1 in intestines
4) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.23
In conclusion, in addition to luminal stimulation of nutrients, a cholinergic impulse as well as peptidergic mediators (among them possibly GIP and GRP) may have an impact on postprandial GLP-1 secretion from the rat ileum.
Localization (secretion) of GLP-1 in ileum
5) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.28
Regulation of glucagon-like peptide-1 secretion from rat ileum by neurotransmitters and peptides.
Localization (secretion) of glucagon-like peptide-1 in ileum associated with neurotransmitter and neuropeptide
6) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Title Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.34
The second incretin hormone, gastric inhibitory polypeptide (GIP), was the most potent stimulant of GLP-1 secretion in our study.
Localization (secretion) of GLP-1
7) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.33
Peptides and neurotransmitters thought to be candidate mediators triggering GLP-1 secretion were arterially infused and GLP-1 was measured in the venous effluent.
Localization (secretion) of GLP-1 associated with neurotransmitter
8) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.31
Arterial infusion of cholinergic agonists strongly enhanced GLP-1 secretion which was counteracted by the addition of atropine.
Localization (secretion) of GLP-1 associated with agonist
9) Confidence 0.80 Published 1995 Journal J. Endocrinol. Section Abstract Doc Link 7490533 Disease Relevance 0 Pain Relevance 0.34
Pirenzepine and gallamine significantly inhibited bethanechol-stimulated GLP-1 secretion, by 96 +/- 12% and 98 +/- 8%, respectively (P < 0.01).
Localization (secretion) of GLP-1
10) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.25
GLP-1 secretion from the distal gut increased 5-fold after 3 ml corn oil were placed into the proximal duodenum (P < 0.001).
Localization (secretion) of GLP-1 in gut
11) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.22
M2 muscarinic receptors also seem to play a role in controlling GLP-1 secretion by fetal, but not adult, L cells.
Localization (secretion) of GLP-1
12) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.15
These results demonstrate the role of M1 muscarinic receptors expressed by L cells in the control of postprandial secretion of GLP-1.
Localization (secretion) of GLP-1
13) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.16
Pirenzepine (an M1 muscarinic receptor antagonist) also inhibited fat-induced GLP-1 secretion in vivo, by 91 +/- 6% (P < 0.01).
Localization (secretion) of GLP-1 in fat associated with antagonist
14) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.27
Atropine (a nonspecific muscarinic receptor antagonist) completely inhibited fat-induced GLP-1 secretion in vivo (P < 0.01).
Localization (secretion) of GLP-1 in fat associated with antagonist
15) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.26
Muscarinic receptors control postprandial release of glucagon-like peptide-1: in vivo and in vitro studies in rats.
Localization (release) of glucagon-like peptide-1 associated with anesthesia
16) Confidence 0.80 Published 2002 Journal Endocrinology Section Title Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.31
Incubating FRIC cultures with bethanechol (a muscarinic receptor agonist) stimulated GLP-1 secretion to 200 +/- 22% of control (P < 0.01).
Localization (secretion) of GLP-1 in FRIC associated with agonist
17) Confidence 0.80 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.26
Secretin or cholecystokinin did not stimulate the secretion of GLP-1.
Localization (secretion) of GLP-1 associated with cholecystokinin
18) Confidence 0.80 Published 1994 Journal Endocrinology Section Abstract Doc Link 7988423 Disease Relevance 0 Pain Relevance 0.33
Intraarterial infusion of glucose-dependent insulinotropic peptide (GIP) over the concentration range 0.25-1 nM evoked a dose-dependent release of GLP-1, with a maximal response of 350% of the basal value.
Localization (release) of GLP-1
19) Confidence 0.80 Published 1994 Journal Endocrinology Section Abstract Doc Link 7988423 Disease Relevance 0 Pain Relevance 0.29
Bombesin (10(-9)-10(-7) M) provoked a dose-dependent release of GLP-1, consisting of an early peak, followed by a sustained response.
Localization (release) of GLP-1
20) Confidence 0.80 Published 1994 Journal Endocrinology Section Abstract Doc Link 7988423 Disease Relevance 0 Pain Relevance 0.33

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