INT115654

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Context Info
Confidence 0.75
First Reported 2004
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 11
Total Number 17
Disease Relevance 3.79
Pain Relevance 2.34

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

signal transduction (Glp1r) plasma membrane (Glp1r) signal transducer activity (Glp1r)
Anatomy Link Frequency
sensory nerves 3
vagus nerve 2
neuronal 2
brain 1
neural 1
Glp1r (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 19 99.26 Very High Very High Very High
vagus nerve 30 98.00 Very High Very High Very High
antagonist 32 97.32 Very High Very High Very High
tolerance 48 97.26 Very High Very High Very High
agonist 31 94.48 High High
Neuropeptide 30 88.40 High High
cva 6 76.24 Quite High
pruritus 12 62.24 Quite High
medulla 12 60.00 Quite High
abdominal pain 6 37.00 Quite Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 630 98.56 Very High Very High Very High
Impaired Glucose Tolerance 42 97.26 Very High Very High Very High
Weight Loss 12 94.68 High High
Hyperglycemia 114 94.00 High High
Hypoglycemia 174 93.72 High High
Targeted Disruption 72 89.68 High High
Cardiovascular Disease 18 86.84 High High
Pulmonary Embolism 6 76.24 Quite High
Heart Rate Under Development 54 75.08 Quite High
Pancreatitis 6 74.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This suggests that GLP-1 could be released in the brain in response to gastric glucose.
Localization (released) of GLP-1 in brain
1) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.39 Pain Relevance 0.08
It is concluded that GLP-1-induced insulin secretion at a low dose in mice is dependent on intact sensory nerves and therefore indirectly mediated and that this distinguishes GLP-1 from other examined insulin secretagogues.
Spec (examined) Localization (secretagogues) of GLP-1 in sensory nerves
2) Confidence 0.73 Published 2004 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Abstract Doc Link 14707011 Disease Relevance 0 Pain Relevance 0.39
It is concluded that GLP-1-induced insulin secretion at a low dose in mice is dependent on intact sensory nerves and therefore indirectly mediated and that this distinguishes GLP-1 from other examined insulin secretagogues.
Localization (secretion) of GLP-1-induced in sensory nerves
3) Confidence 0.69 Published 2004 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Abstract Doc Link 14707011 Disease Relevance 0 Pain Relevance 0.43
Sensory nerves contribute to insulin secretion by glucagon-like peptide-1 in mice.
Localization (secretion) of glucagon-like peptide-1 in Sensory nerves associated with qutenza
4) Confidence 0.69 Published 2004 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Title Doc Link 14707011 Disease Relevance 0 Pain Relevance 0.43
GLP-1 is also secreted by neuronal cells from the caudal region of the brain stem, the nucleus of the tractus solitarius (NTS) (15,16), and released in various hypothalamic, hippocampal, and cortical nuclei, areas that contain functional GLP-1Rcs (15,17–22).
Localization (released) of GLP-1 in neuronal
5) Confidence 0.66 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.09 Pain Relevance 0.17
Endogenously secreted GLP-1 acts in the hepatic portal vein to increase the firing rate of the vagus nerve (10,11) and regulate glucose metabolism (12–14).
Localization (secreted) of GLP-1 in vagus nerve associated with vagus nerve
6) Confidence 0.66 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.10 Pain Relevance 0.19
GLP-1 is also secreted by neuronal cells from the caudal region of the brain stem, the nucleus of the tractus solitarius (NTS) (15,16), and released in various hypothalamic, hippocampal, and cortical nuclei, areas that contain functional GLP-1Rcs (15,17–22).
Localization (secreted) of GLP-1 in neuronal
7) Confidence 0.66 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.09 Pain Relevance 0.17
GLP-1 is secreted by enteroendocrine L cells and enhances glucose-stimulated insulin secretion (9).
Localization (secreted) of GLP-1
8) Confidence 0.66 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.08 Pain Relevance 0.16
GLP-1 is released into the portal vein and controls the firing rate of the vagus nerve (32) and the hepatoportal sensor system, leading to an increased whole-body glucose utilization rate (14).
Localization (released) of GLP-1 in vagus nerve associated with vagus nerve
9) Confidence 0.66 Published 2008 Journal Diabetes Section Body Doc Link PMC2551668 Disease Relevance 0.06 Pain Relevance 0.12
We therefore conclude that PDE3 inhibition by milrinone augments insulin secretion in vivo in mice after oral but not after intravenous glucose, which may be explained by enhanced response to the cAMP-dependent insulinotropic action of endogenously released GLP-1.
Localization (released) of GLP-1
10) Confidence 0.62 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15364011 Disease Relevance 0 Pain Relevance 0
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 Glucagon-like peptide-1 in intestine
11) Confidence 0.43 Published 2005 Journal Endocrinology Section Abstract Doc Link 15932924 Disease Relevance 0 Pain Relevance 0.04
GLP-1 is secreted from the L-cells in the distal small intestine/colon in response to mixed meals (glucose or fat).
Localization (secreted) of GLP-1 in fat
12) Confidence 0.15 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.35 Pain Relevance 0
Thus, the secreted GLP-1 and GIP have a short half-life in the range of 2–3 minutes.
Localization (secreted) of GLP-1
13) Confidence 0.15 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.47 Pain Relevance 0.05
These clinical observations reinforce the mechanism of action of endogenously-secreted GLP-1 on insulin secretion as being glucose-dependent and demonstrate that, when the DPP-4 inhibitor alogliptin is administered with agents that do not augment insulin secretion, hypoglycemia is uncommon and does not occur more frequently than in the placebo group.
Localization (secreted) of GLP-1 associated with hypoglycemia
14) Confidence 0.15 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 1.01 Pain Relevance 0.07
Circulating concentrations of GLP-1 rise rapidly within minutes after food ingestion indicating that neural signals, initiated by food entry in the proximal gastrointestinal tract, stimulate GLP-1 secretion via the L-cells.87 Acutely, GLP-1 promotes normal glucose homeostasis by augmenting insulin secretion, inhibiting glucagon secretion and delaying gastric emptying.
Localization (secretion) of GLP-1 in neural
15) Confidence 0.15 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.27 Pain Relevance 0
The incretin effect accounts for approximately 70% of all insulin that is secreted during an OGTT in normal glucose tolerant subjects,86 and GLP-1 and glucose-dependent insulinotrophic polypeptide (previously called gastric inhibitory polypeptide, GIP) account for over 90% of the incretin effect.
Localization (secreted) of GLP-1
16) Confidence 0.14 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.40 Pain Relevance 0
As individuals progress from normal glucose tolerance to IGT to T2DM, stimulated GLP-1 levels decline89,90 (Figure 7), and there is beta cell resistance to the glucose-dependent stimulatory effect of both GLP-1 and GIP on insulin secretion.91 In T2DM the contribution of incretin hormones to the insulin response has been estimated to be reduced to about 36% in T2DM subjects.86,92 From the therapeutic standpoint, one can increase circulating GLP-1 levels by administering a GLP-1 analog that is resistant to DPP-4 degradation or by giving a DPP-4 inhibitor.7,93,94
Localization (effect) of GLP-1 in beta cell associated with diabetes mellitus, tolerance and impaired glucose tolerance
17) Confidence 0.14 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.47 Pain Relevance 0.05

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