INT145450

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.79
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 17
Disease Relevance 0.75
Pain Relevance 1.14

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 2
ileum 1
fat 1
vagal nerve 1
epithelium 1
Pyy (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 220 99.12 Very High Very High Very High
Bile 5 99.00 Very High Very High Very High
Neurotransmitter 16 88.04 High High
Neuropeptide 21 87.36 High High
Cholecystokinin 6 79.28 Quite High
qutenza 23 70.36 Quite High
tolerance 176 69.36 Quite High
nerve block 11 68.08 Quite High
agonist 223 61.04 Quite High
Potency 22 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Constipation 22 97.90 Very High Very High Very High
Targeted Disruption 97 96.88 Very High Very High Very High
Adhesions 5 81.84 Quite High
Disorder Of Lipid Metabolism 2 81.36 Quite High
Impaired Glucose Tolerance 176 70.00 Quite High
Obesity 16 61.76 Quite High
Hyperinsulinism 5 48.16 Quite Low
Stress 22 23.56 Low Low
Diabetes Mellitus 27 8.72 Low Low
Body Weight 16 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Anatomical and functional studies have shown that Y1 receptors are targeted to basolateral epithelial membranes (Mannon et al., 1999; Cox and Tough, 2002) and would therefore be activated by endogenous PYY or NPY released into the subepithelial area.
Localization (released) of PYY
1) Confidence 0.79 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.05
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 PYY
2) Confidence 0.74 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0
We therefore conclude that antidiabetic DPP-IV inhibitors such as vildagliptin may cause constipation, as has been observed clinically (Lauster et al., 2007), but that this is unlikely to involve increased stability of PYY.
Localization (stability) of PYY associated with constipation
3) Confidence 0.74 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.22 Pain Relevance 0.06
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 PYY in colon associated with antagonist
4) Confidence 0.74 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.23
For PYY release, mucosae were incubated in 2 ml KH buffer at 37°C with either vehicle (1% DMSO) or tolbutamide (1 mM) for 90 min.
Localization (release) of PYY
5) Confidence 0.70 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.06 Pain Relevance 0.16
PYY was released from WT colonic mucosa treated with tolbutamide, but not from vehicle controls, and WT tissue total PYY levels were not altered significantly (Figure S3D).
Localization (released) of PYY
6) Confidence 0.64 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 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).
Localization (coreleased) of PYY in ileum
7) Confidence 0.64 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.09
Dietary fat, bile salts, carbohydrates, and proteins can stimulate PYY release but to different degrees and with different rates (for review, see Onaga et al. [15]).
Localization (release) of PYY in bile associated with bile
8) Confidence 0.61 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0 Pain Relevance 0.09
PYY release is also regulated by, and in turn regulates, vagal nerve activity [15] and the hormone is a major mediator of ileal and colonic brakes, mechanisms that ultimately slow gastric emptying and promote digestive activities to increase nutrient absorption [16–18].
Localization (release) of PYY in vagal nerve
9) Confidence 0.61 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0 Pain Relevance 0.09
Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear.
Localization (released) of PYY
10) Confidence 0.61 Published 2010 Journal Cell Metabolism Section Abstract Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0
Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear.
Localization (released) of Peptide YY
11) Confidence 0.61 Published 2010 Journal Cell Metabolism Section Abstract Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0
Changes in PYY release were compared using Student's paired t test, and in all cases p ?
Localization (release) of PYY
12) Confidence 0.61 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0.07 Pain Relevance 0.03
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?
Localization (use) of PYY
13) Confidence 0.50 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0.10 Pain Relevance 0
Ultimately, whatever the luminal or neural (vagal) stimulus, released PYY will rapidly activate several local (paracrine) targets, primary among them, the epithelium.
Localization (released) of PYY in epithelium
14) Confidence 0.47 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0.14 Pain Relevance 0
Peptide YY (PYY)(3-36), released by intestinal lipid elicits functional effects that comprise the intestinal feedback response to luminal nutrients, but the pathway of action is not fully characterized.
Localization (released) of PYY
15) Confidence 0.41 Published 2007 Journal Endocrinology Section Abstract Doc Link 17641001 Disease Relevance 0.16 Pain Relevance 0.12
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 PYY in colon
16) Confidence 0.22 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2890049 Disease Relevance 0 Pain Relevance 0.09
Dietary fat, bile salts, carbohydrates, and proteins can stimulate PYY release but to different degrees and with different rates (for review, see Onaga et al. [15]).
Localization (release) of PYY in fat associated with bile
17) Confidence 0.21 Published 2008 Journal Nutrition Section Body Doc Link PMC2572019 Disease Relevance 0 Pain Relevance 0.09

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox