INT127524

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Context Info
Confidence 0.53
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 16
Disease Relevance 4.28
Pain Relevance 1.70

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

nucleus (Zglp1) DNA binding (Zglp1)
Anatomy Link Frequency
colon 2
gut 2
ileum 1
hypothalamus 1
inferior 1
Zglp1 (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 136 99.60 Very High Very High Very High
antagonist 128 99.12 Very High Very High Very High
Neuropeptide 18 96.16 Very High Very High Very High
agonist 382 92.36 High High
Neurotransmitter 8 88.72 High High
Intracerebroventricular 24 84.56 Quite High
abdominal pain 4 79.20 Quite High
nerve block 8 78.96 Quite High
withdrawal 4 72.52 Quite High
Central nervous system 12 52.56 Quite High
Disease Link Frequency Relevance Heat
Impaired Glucose Tolerance 136 99.60 Very High Very High Very High
Weight Gain 16 99.20 Very High Very High Very High
Diabetes Mellitus 437 98.84 Very High Very High Very High
Hyperglycemia 68 98.40 Very High Very High Very High
Diarrhoea 8 97.12 Very High Very High Very High
Constipation 20 96.60 Very High Very High Very High
Hypoglycemia 123 96.20 Very High Very High Very High
Vomiting 40 90.24 High High
Pressure And Volume Under Development 20 87.08 High High
Appetite Loss 6 80.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
GLP-1 is released into the hypothalamus and controls food intake, blood pressure, and heart rate (9,10).
Localization (released) of GLP-1 in hypothalamus
1) Confidence 0.53 Published 2008 Journal Diabetes Section Body Doc Link PMC2551665 Disease Relevance 0.26 Pain Relevance 0.10
In our experimental procedure, hyperglycemia was induced by a systemic glucose infusion; therefore, under these conditions, GLP-1 secretion from the gut is not increased.
Localization (secretion) of GLP-1 in gut associated with hyperglycemia
2) Confidence 0.53 Published 2008 Journal Diabetes Section Body Doc Link PMC2551665 Disease Relevance 0.40 Pain Relevance 0.26
GLP-1 is a gut hormone secreted in response to oral glucose absorption that regulates glucose metabolism and cardiovascular function.
Localization (secreted) of GLP-1 in gut
3) Confidence 0.50 Published 2008 Journal Diabetes Section Abstract Doc Link PMC2551665 Disease Relevance 0 Pain Relevance 0.04
Glucagon-like peptide-1(7-36NH2) (GLP-1) and peptide YY(3-36NH2) (PYY(3-36NH2)) are cosecreted from the intestine in response to nutrient ingestion.
Localization (cosecreted) of GLP-1 in intestine
4) Confidence 0.24 Published 2005 Journal Endocrinology Section Abstract Doc Link 15932924 Disease Relevance 0 Pain Relevance 0.04
The endogenous Gpr119 ligand, oleoylethanolamide (OEA), has been shown to reduce food intake and weight gain (Overton et al., 2006) and to increase GLP-1 release from L cells in vitro and in vivo (Ahrén et al., 2004; Reimann et al., 2008).
Localization (release) of GLP-1 associated with weight gain
5) Confidence 0.22 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.19 Pain Relevance 0.04
This L cell mechanism is similar to that described recently for GLP-1 release from isolated L cells (Lauffer et al., 2009; Tolhurst et al., 2009), with the notable difference being that Gpr119 receptors are present within both apical and basolateral membranes of intact tissue where epithelial polarity is maintained.
Localization (release) of GLP-1
6) Confidence 0.20 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.14 Pain Relevance 0.07
Enteroendocrine L cells located predominantly in the distal ileum and colon of human and rodent intestine (Böttcher et al., 1984; Arantes and Nogueira, 1997) are the primary source of PYY, which is coreleased following food intake with proglucagon products, GLP-1 and GLP-2 (Gardiner et al., 2008).
Localization (coreleased) of GLP-1 in ileum
7) Confidence 0.20 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.09
While local GLP-1 and PYY activities differ, e.g., the former modulating epithelial barrier function rather than modulating epithelial anion secretion, the repertoire of GLP-1 and PYY hormonal activities match more closely, e.g., both reduce gastric emptying, inhibit intestinal motility, and modulate vagal afferent output (Drucker, 2005; Dockray, 2009).
Localization (local) of GLP-1
8) Confidence 0.20 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0
This response was abolished by the GLP-1 receptor antagonist exendin(9-39) (Figure 2E), indicating that corelease of endogenous GLP-1 with PYY occurs in human colon mucosa following Gpr119 stimulation.
Localization (corelease) of GLP-1 in colon associated with antagonist
9) Confidence 0.20 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.23
As Gpr119 is expressed in L cells that contain GLP-1, it has been hypothesized that Gpr119 agonism may improve glucose tolerance via stimulation of GLP-1 release, as recently reviewed (Overton et al., 2008).
Localization (release) of GLP-1 associated with tolerance and impaired glucose tolerance
10) Confidence 0.19 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.39 Pain Relevance 0.16
Only when the Y1 and Y2 receptors were blocked was the small GLP-1 secretory (presumably G?
Localization (secretory) of small GLP-1
11) Confidence 0.18 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.23
g bid.84 In most patients the frequency, and severity, peaks in the first 8 weeks of treatment and decreases thereafter,64,66 and is likely to be a central GLP-1 effect, unrelated to the slowing of gastric emptying.84 Other GI AEs, such as diarrhea and constipation, are less common, and are also usually transient and mild.
Localization (effect) of GLP-1 associated with constipation and diarrhoea
12) Confidence 0.11 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2731024 Disease Relevance 1.22 Pain Relevance 0.16
Sitagliptin (Januvia®; Merck and Co, Inc.) was approved for use in a dose of 100 mg once daily, by the FDA in 2006 and subsequently in the EU, Australia and Asia, for the improvement of glycemic control in combination with metformin and/or a sulfonylurea when diet and exercise plus OHA do not result in adequate glycemic control.96 In drug-naïve T2DM patients, sitagliptin monotherapy is more effective than placebo in reducing HbA1c (by up to 1%) and fasting glucose (by up to 18 mg/dL).97 Greater benefits in glycemic control were seen with sitagliptin 100 mg daily, compared to placebo, over a period of 24 weeks in T2DM patients already on metformin98,99 and pioglitazone,100 and when added to sulfonylureas (with or without metformin).101 It was non-inferior to glipizide when added to ongoing metformin therapy.102 Metformin stimulates GLP-1 release, increasing both active and total GLP-1 levels by 2-fold, but does not act as a DPP-4 inhibitor, and, accordingly, has a synergistic effect with sitagliptin, to increase both active GLP-1 (?
Localization (release) of GLP-1 in inferior associated with diabetes mellitus
13) Confidence 0.11 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2731024 Disease Relevance 0.25 Pain Relevance 0.03
In T2DM patients during hyperglycemic clamp studies, infusion of GLP-1, but not GIP, stimulates insulin secretion,19 establishing that the insulinotropic effect of GLP-1 is relatively well-preserved in T2DM, despite possibly lower levels, when compared to non-diabetic subjects.20 On the other hand, GIP levels are essentially normal in T2DM but GIP-stimulated second-phase insulin secretion is markedly diminshed21 (although it has recently been reported that reversal of poor glycemic control in T2DM improves the insulin response to both GIP and GLP-1).21 Hence, the development of incretin-based therapies for T2DM has hitherto focused on GLP-1, rather than GIP.
Localization (secretion) of GLP-1 associated with diabetes mellitus
14) Confidence 0.11 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2731024 Disease Relevance 0.98 Pain Relevance 0
Albiglutide, a DPP-4-resistant GLP-1 analog which is administered weekly, reduced fasting and postprandial glucose levels without causing hypoglycemia in healthy subjects87 and T2DM patients.88 A dose of 32 mg reduced 24-hour mean weighted glucose by 35 mg/dL (?
Localization (analog) of GLP-1 associated with hypoglycemia and diabetes mellitus
15) Confidence 0.10 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2731024 Disease Relevance 0.45 Pain Relevance 0.16
Enteroendocrine L cells located predominantly in the distal ileum and colon of human and rodent intestine (Böttcher et al., 1984; Arantes and Nogueira, 1997) are the primary source of PYY, which is coreleased following food intake with proglucagon products, GLP-1 and GLP-2 (Gardiner et al., 2008).
Localization (coreleased) of GLP-1 in colon
16) Confidence 0.07 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.09

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