INT59737

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Context Info
Confidence 0.43
First Reported 1993
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 15
Total Number 15
Disease Relevance 6.94
Pain Relevance 2.01

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
plasma 3
proximal 2
lung 1
Glp1r (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Somatostatin 8 100.00 Very High Very High Very High
Potency 3 99.92 Very High Very High Very High
qutenza 4 99.20 Very High Very High Very High
Chronic pancreatitis 7 98.12 Very High Very High Very High
antagonist 12 96.56 Very High Very High Very High
vagus nerve 2 94.96 High High
substance P 6 80.32 Quite High
Clonidine 1 78.96 Quite High
agonist 14 78.56 Quite High
Neuropeptide 2 75.00 Quite High
Disease Link Frequency Relevance Heat
Body Weight 28 99.88 Very High Very High Very High
Diabetes Mellitus 143 99.52 Very High Very High Very High
Pancreatitis 8 98.12 Very High Very High Very High
Obesity 18 96.36 Very High Very High Very High
Hypertension 8 95.20 Very High Very High Very High
Aging 2 92.56 High High
Hypoglycemia 7 91.98 High High
Hyperlipidemia 10 91.92 High High
Gastric Fistula 1 87.68 High High
Insulin Resistance 25 86.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Exogenous administration of glucagon-like peptide-1-(7-36) amide (GLP-1), an insulinotropic hormone, inhibits gastric emptying and acid secretion in humans.
Negative_regulation (administration) of GLP-1
1) Confidence 0.43 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9357836 Disease Relevance 0.09 Pain Relevance 0.08
Plasma levels of glucagon-like peptide-1 (GLP-1) rise rapidly after nutrient ingestion through an indirect mechanism triggered from the proximal intestine and involving the vagus nerve that stimulates the L cell in the distal gut.
Negative_regulation (levels) of GLP-1 in proximal associated with vagus nerve
2) Confidence 0.43 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.10
Plasma levels of glucagon-like peptide-1 (GLP-1) rise rapidly after nutrient ingestion through an indirect mechanism triggered from the proximal intestine and involving the vagus nerve that stimulates the L cell in the distal gut.
Negative_regulation (levels) of glucagon-like peptide-1 in proximal associated with vagus nerve
3) Confidence 0.43 Published 2002 Journal Endocrinology Section Abstract Doc Link 12021207 Disease Relevance 0 Pain Relevance 0.08
MATERIALS AND METHODS: The overall metabolism of GLP-1 and exendin-4 was directly compared in anaesthetised pigs (n=9).
Negative_regulation (metabolism) of GLP-1
4) Confidence 0.38 Published 2006 Journal Diabetologia Section Body Doc Link 16447056 Disease Relevance 0 Pain Relevance 0
Because body weight also decreased in the GLP-1 and AC3174 groups, the ratios of LV, RV, and lung to body weight did not reach significance for all doses of GLP-1 and AC3174, although lung weight was reduced at the higher doses of both agents.
Negative_regulation (decreased) of GLP-1 in lung associated with body weight
5) Confidence 0.36 Published 2010 Journal Cardiovasc Diabetol Section Body Doc Link PMC2996354 Disease Relevance 0.83 Pain Relevance 0.03
In conclusion, 1) high levels of gene expression and secretion of NPY are found in a rat insulinoma cell line (INS-1). 2) Accumulation of cAMP induced by forskolin or a gluco-incretin (GLP-1) induces a further increase in NPY gene expression and release. 3) NPY secretion is not modulated by low or high glucose concentrations in the medium. 4) Induction of NPY, a known inhibitor of insulin secretion, may represent a novel counterregulatory mechanism of insulin secretion, limiting the stimulatory effect of GLP-1 on insulin secretion.
Negative_regulation (effect) of GLP-1 associated with hypoglycemia
6) Confidence 0.20 Published 1993 Journal Endocrinology Section Abstract Doc Link 8396008 Disease Relevance 0.14 Pain Relevance 0.16
The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients.
Negative_regulation (evaluate) of GLP-1 in plasma associated with diabetes mellitus and obesity
7) Confidence 0.17 Published 2003 Journal J. Clin. Endocrinol. Metab. Section Abstract Doc Link 14557471 Disease Relevance 1.15 Pain Relevance 0.08
GLP-1 secretion, on the other hand, is also impaired, but its insulinotropic and glucagon-suppressive actions are preserved, although the potency of GLP-1 in this respect is decreased compared to healthy subjects.
Negative_regulation (decreased) of GLP-1 associated with potency
8) Confidence 0.15 Published 2009 Journal Mol. Cell. Endocrinol. Section Abstract Doc Link 18786605 Disease Relevance 0.76 Pain Relevance 0.14
The impaired action of GLP-1 and GIP in T2DM may be at least partly restored by improved glycaemic control, as shown in studies involving 4 weeks of intensive insulin therapy.
Negative_regulation (impaired) of GLP-1 associated with diabetes mellitus
9) Confidence 0.15 Published 2009 Journal Mol. Cell. Endocrinol. Section Abstract Doc Link 18786605 Disease Relevance 0.76 Pain Relevance 0.13
The two main categories of incretin therapy currently available are: glucagon-like peptide-1 (GLP-1) analogues and inhibitors of GLP-1 degrading enzyme dipeptidyl peptidase-4 (DPP-4).
Negative_regulation (inhibitors) of GLP-1
10) Confidence 0.14 Published 2008 Journal Drugs Aging Section Abstract Doc Link 18947259 Disease Relevance 0.99 Pain Relevance 0.07
Future studies from us will estimate the effects of this DPP-IV inhibitor on the enzyme activity/expression, as well as on levels of GLP-1 and glucagon, in order to have a more detailed picture of how the incretins pathway is affected and its relative contribution for the effects of sitagliptin here reported.
Negative_regulation (inhibitor) of GLP-1
11) Confidence 0.13 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2905949 Disease Relevance 1.00 Pain Relevance 0
OBJECTIVE: The purpose of the present study was to evaluate plasma glucagon-like peptide-1 (GLP-1) responses after oral glucose ingestion in patients with chronic pancreatitis and to clarify how GLP-1 secretion relates to pancreatic diabetes.
Negative_regulation (evaluate) of glucagon-like peptide-1 in plasma associated with diabetes mellitus and chronic pancreatitis
12) Confidence 0.10 Published 1999 Journal Am. J. Gastroenterol. Section Abstract Doc Link 10201468 Disease Relevance 0.27 Pain Relevance 0.10
OBJECTIVE: The purpose of the present study was to evaluate plasma glucagon-like peptide-1 (GLP-1) responses after oral glucose ingestion in patients with chronic pancreatitis and to clarify how GLP-1 secretion relates to pancreatic diabetes.
Negative_regulation (evaluate) of GLP-1 in plasma associated with diabetes mellitus and chronic pancreatitis
13) Confidence 0.10 Published 1999 Journal Am. J. Gastroenterol. Section Abstract Doc Link 10201468 Disease Relevance 0.27 Pain Relevance 0.10
In particular, we highlight the efficacy and safety of GLP-1 and DPP-4 inhibitors, administered as monotherapy or in combination with other oral antihyperglycaemic agents, especially when the relevant clinical trials included older persons.
Negative_regulation (inhibitors) of GLP-1
14) Confidence 0.10 Published 2008 Journal Drugs Aging Section Abstract Doc Link 18947259 Disease Relevance 0.69 Pain Relevance 0.05
Simultaneous addition of receptor antagonists to all three tachykinin receptors (CP96345, SR48968, and SR142801, all at 10(-6) M) significantly inhibited the effect of capsaicin on VIP release, whereas the release of GLP-1 and somatostatin was unaffected.
Negative_regulation (unaffected) of GLP-1 associated with qutenza, antagonist and somatostatin
15) Confidence 0.03 Published 1999 Journal Dig. Dis. Sci. Section Abstract Doc Link 10489905 Disease Relevance 0 Pain Relevance 0.88

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