INT128369

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Context Info
Confidence 0.79
First Reported 2005
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 27
Total Number 29
Disease Relevance 10.39
Pain Relevance 7.06

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

cell proliferation (PYY) extracellular space (PYY) extracellular region (PYY)
cytoskeleton organization (PYY) cell-cell signaling (PYY)
Anatomy Link Frequency
plasma 7
ileum 5
small intestine 3
proximal 3
intestine 1
PYY (Homo sapiens)
Pain Link Frequency Relevance Heat
Cholecystokinin 1806 100.00 Very High Very High Very High
Dopamine 7 94.72 High High
opiate 1 94.20 High High
Opioid 38 90.80 High High
Neuropeptide 26 90.76 High High
cytokine 57 90.44 High High
Inflammation 545 90.04 High High
antagonist 87 87.24 High High
Endocannabinoid 15 80.68 Quite High
Serotonin 7 79.20 Quite High
Disease Link Frequency Relevance Heat
Critical Illness 1145 99.84 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 18 99.54 Very High Very High Very High
Shock 13 99.16 Very High Very High Very High
Gastric Motility Disorder 104 96.40 Very High Very High Very High
Increased Venous Pressure Under Development 13 95.52 Very High Very High Very High
Appetite Loss 77 95.36 Very High Very High Very High
Pressure And Volume Under Development 22 93.36 High High
Hypoglycemia 12 93.28 High High
INFLAMMATION 605 90.04 High High
Obesity 390 87.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Currently, there are no data on the impact of insulin on the release of CCK or PYY in humans.
Localization (release) of PYY associated with cholecystokinin
1) Confidence 0.79 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.27 Pain Relevance 0.27
Consistent with our recent study [29], the postprandial release of PYY is related to the release of CCK, which supports the concept that CCK is an important proximal mediator for the release of PYY [9,10].
Localization (release) of PYY in proximal associated with cholecystokinin
2) Confidence 0.79 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.17 Pain Relevance 0.20
For example, in response to duodenal nutrient, there is a greater degree of antral hypo-motility, pyloric hyperactivity [27], and exaggerated release of both CCK and PYY in critically ill patients [28,29].
Localization (release) of PYY associated with critical illness, attention deficit hyperactivity disorder and cholecystokinin
3) Confidence 0.79 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.58 Pain Relevance 0.32
Furthermore, evidence from animal studies [49] suggests that PYY may be released by direct neural stimulation from nutrients in the proximal intestine, possibly via a neural linkage between the proximal gut to the distal PYY-secreting cells which involves sensory vagal fibres with nicotinic, beta-adrenergic, opioid, and serotonergic synapses and nitric oxide release [49,50].
Localization (released) of PYY in proximal associated with opioid
4) Confidence 0.79 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.21 Pain Relevance 0.22
This observation is at variance with recent findings that suggest that critically ill patients with feed intolerance have higher plasma CCK and PYY release in response to duodenal nutrients than patients who tolerated feeds [28,29].
Localization (release) of PYY in plasma associated with critical illness and cholecystokinin
5) Confidence 0.79 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.27 Pain Relevance 0.20
There was a trend for higher plasma PYY concentrations in patients who received inotropic therapy, but whether the elevation is a physiological response to shock or a direct effect of inotropic drugs on PYY release is unknown.
Localization (release) of PYY in plasma associated with shock
6) Confidence 0.75 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.49 Pain Relevance 0.11
Because prolonged small intestinal transit is common in critically ill patients [27,28], it is unlikely that nutrients would have reached the distal ileum within 60 minutes for direct stimulation of PYY release.
Localization (release) of PYY in ileum associated with critical illness
7) Confidence 0.75 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.50 Pain Relevance 0.09
In animals, PYY release in response to intestinal nutrients cannot be abolished by preventing nutrient delivery to the site of PYY-containing cells in the distal ileum, but only by removing these cells completely (that is, ileo-colectomy) [31].
Localization (release) of PYY in ileum
8) Confidence 0.75 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.61 Pain Relevance 0.63
PYY release from the distal small intestine is stimulated both directly by luminal nutrients, particularly the digestion products of fat which activate PYY-secreting cells [7], and indirectly by neuro-endocrine mechanisms, including the release of cholecystokinin (CCK) and insulin-like growth factor-1 [8].
Localization (release) of PYY in fat associated with cholecystokinin
9) Confidence 0.75 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0 Pain Relevance 0.17
The major observations are that, during critical illness, (a) GE was inversely related to both fasting and postprandial plasma CCK and PYY concentrations but (b) the postprandial increases in plasma CCK and PYY were also directly related to GE.
Localization (related) of PYY in plasma associated with critical illness and cholecystokinin
10) Confidence 0.74 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.43 Pain Relevance 0.43
Measurement of plasma PYY and CCK concentrations
Localization (Measurement) of plasma PYY in plasma associated with cholecystokinin
11) Confidence 0.70 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.06 Pain Relevance 0.10
In response to the presence of nutrients (particularly fat and protein) in the small intestine, CCK and PYY are released in a load-dependent manner from enteroendocrine cells, predominantly in the proximal small intestine for CCK and the distal small intestine for PYY [5-8].
Localization (released) of PYY in small intestine associated with cholecystokinin
12) Confidence 0.69 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0 Pain Relevance 0.37
Consistent with our recent study [29], the postprandial release of PYY is related to the release of CCK, which supports the concept that CCK is an important proximal mediator for the release of PYY [9,10].
Localization (release) of PYY in proximal associated with cholecystokinin
13) Confidence 0.69 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.21 Pain Relevance 0.21
Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake.
Localization (released) of peptide YY in digestive tract associated with cholecystokinin
14) Confidence 0.68 Published 2005 Journal Basic Clin. Pharmacol. Toxicol. Section Abstract Doc Link 15998351 Disease Relevance 0.20 Pain Relevance 0.28
These findings are consistent with the concept that the sensitivity of the small intestine to PYY release is increased in critical illness and suggest a potential contribution of this hormone to delayed gastric emptying.
Localization (release) of PYY in small intestine associated with critical illness and gastric motility disorder
15) Confidence 0.66 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.56 Pain Relevance 0.21
The lack of a dose-dependent response to nutrients in critically ill patients is consistent with the concept that the 'sensitivity' of the small intestine to PYY release is enhanced.
Localization (release) of PYY in small intestine associated with critical illness
16) Confidence 0.66 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.94 Pain Relevance 0
This elevated response is strongly related to plasma CCK concentrations, suggesting an important role for this hormone in mediating increased PYY release.
Localization (release) of PYY in plasma associated with cholecystokinin
17) Confidence 0.66 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.80 Pain Relevance 0.12
It is also possible that direct neural stimulation in the proximal intestine triggers the release of PYY from the distal ileum [30-32].
Localization (release) of PYY in intestine
18) Confidence 0.65 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.68 Pain Relevance 0.67
Furthermore, because the release of PYY is influenced by CCK, an elevated response would be associated with enhanced CCK secretion.


Localization (release) of PYY associated with cholecystokinin
19) Confidence 0.65 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.61 Pain Relevance 0.28
CCK appears to be an important 'proximal' mediator in that (a) it stimulates the release of PYY [8], (b) fasting and nutrient-stimulated plasma CCK are elevated in the critically ill [19], and (c) both fasting and nutrient-stimulated plasma PYY concentrations correlate strongly with CCK.
Localization (release) of PYY in plasma associated with critical illness and cholecystokinin
20) Confidence 0.65 Published 2006 Journal Crit Care Section Body Doc Link PMC1794491 Disease Relevance 0.58 Pain Relevance 0.28

General Comments

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