INT145449

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Context Info
Confidence 0.77
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 12
Disease Relevance 0.74
Pain Relevance 1.36

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

extracellular space (Pyy) extracellular region (Pyy)
Anatomy Link Frequency
colon 3
ileum 1
bowel 1
large intestine 1
Pyy (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 172 97.08 Very High Very High Very High
antagonist 149 96.44 Very High Very High Very High
qutenza 19 95.84 Very High Very High Very High
Cholecystokinin 6 94.44 High High
Neurotransmitter 11 93.60 High High
Neuropeptide 13 91.92 High High
Potency 18 89.12 High High
member 8 9 72.16 Quite High
tolerance 144 62.00 Quite High
tetrodotoxin 13 49.24 Quite Low
Disease Link Frequency Relevance Heat
Targeted Disruption 71 96.88 Very High Very High Very High
Weight Gain 9 78.48 Quite High
Disorder Of Lipid Metabolism 2 75.00 Quite High
Hyperinsulinism 2 73.64 Quite High
Obesity 11 66.48 Quite High
Impaired Glucose Tolerance 144 62.64 Quite High
Adhesions 2 56.48 Quite High
Body Weight 11 21.20 Low Low
Diabetes Mellitus 20 5.00 Very Low Very Low Very Low
Stress 18 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As the expression pattern of Gpr119 in the GI tract closely resembles that of PYY-expressing L cells, we chose to activate Gpr119 receptors using the small molecule agonist, PSN632408, which is less lipophilic and more selective for Gpr119 than OEA.
Gene_expression (expressing) of PYY associated with agonist
1) Confidence 0.77 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.23
In contrast, PYY responses per se were not glucose sensitive, nor were the antisecretory effects of the ?
Gene_expression (responses) of PYY
2) Confidence 0.66 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.05
In particular, the expression pattern of Gpr119 is very similar to that of PYY/GLP-1 containing L cells (Chu et al., 2008), suggesting that Gpr119 stimulation could cause significant PYY-related responses as well as GLP-1-mediated effects in the colon and elsewhere.
Gene_expression (containing) of PYY in colon
3) Confidence 0.66 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.14 Pain Relevance 0.06
The PYY-synthesizing L-cells of the large bowel play a pivotal role, not only in the regulation of satiety and ileal brake but also in response to different luminal cues, e.g., fatty acid chain length [33], resulting in predominant Y1 absorptive responses.
Gene_expression (synthesizing) of PYY in bowel
4) Confidence 0.59 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0.20 Pain Relevance 0.05
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).
Gene_expression (source) of PYY in ileum
5) Confidence 0.58 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.08
Together with PP and the dipeptidylpeptidase IV (DPP-IV)-cleaved products NPY(3-36) and PYY(3-36) (Mentlein et al., 1993), NPY and PYY exert a range of inhibitory activities, such as slowing gastric emptying, reducing intestinal anion and electrolyte secretion (Playford et al., 1990; Cox and Tough, 2002), and slowing intestinal motility, which collectively promote nutrient absorption.
Gene_expression (products) of PYY
6) Confidence 0.58 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.09
To establish the link between Gpr119 and endogenous PYY or NPY function in colon mucosa, we tested PSN632408 in the absence or presence of selective Y receptor antagonists.
Gene_expression (function) of PYY in colon associated with antagonist
7) Confidence 0.58 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.09 Pain Relevance 0.19
A similar increasing sensitivity to exogenous PYY and NPY has also been described from the small to the large intestine of the mouse (Cox et al., 2001).
Gene_expression (exogenous) of PYY in large intestine
8) Confidence 0.58 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.08 Pain Relevance 0
This demonstrates that ablation of PYY or selective blockade of epithelial Y1 receptors (Figure 2B) renders colonic mucosa insensitive to Gpr119 activation, confirming the functional requirement of Gpr119 mucosal signaling for endogenous PYY.
Gene_expression (mucosal) of PYY
9) Confidence 0.58 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.10
Therefore, we set out to establish whether endogenous PYY was responsible for Y1 absorptive tone and NPY-mediated Y2 tone, making use of single (PYY?
Gene_expression (single) of PYY
10) Confidence 0.45 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0.10 Pain Relevance 0
PYY(3-36)-induced Fos expression was significantly reduced by 65% in A-IV(+/+) mice pretreated systemically with the sensory neurotoxin capsaicin (5 mg/100 g), 78% by the CCK(1)R antagonist, devazepide (10 microg/100 g), and 39% by the Y2R antagonist, BIIE0246 (200 and 600 microg/100 g) and decreased by 67% in apo A-IV(-/-) mice, compared with A-IV(+/+) controls.
Gene_expression (expression) of PYY associated with qutenza, antagonist and cholecystokinin
11) Confidence 0.35 Published 2007 Journal Endocrinology Section Abstract Doc Link 17641001 Disease Relevance 0.14 Pain Relevance 0.42
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).
Gene_expression (source) of PYY in colon
12) Confidence 0.20 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.08

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