INT98773

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Context Info
Confidence 0.53
First Reported 2001
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 10
Total Number 25
Disease Relevance 9.59
Pain Relevance 1.50

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 (Gcg) extracellular region (Gcg) cytoplasm (Gcg)
Anatomy Link Frequency
plasma 8
lung 6
alpha cell 4
external 2
neural 2
Gcg (Mus musculus)
Pain Link Frequency Relevance Heat
Clonidine 6 99.56 Very High Very High Very High
agonist 64 96.24 Very High Very High Very High
Action potential 12 94.64 High High
Paracetamol 52 84.08 Quite High
tolerance 112 83.12 Quite High
tetrodotoxin 4 56.16 Quite High
Inflammation 80 5.00 Very Low Very Low Very Low
pruritus 32 5.00 Very Low Very Low Very Low
headache 32 5.00 Very Low Very Low Very Low
Neuropeptide 16 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 1522 99.80 Very High Very High Very High
Gastric Motility Disorder 16 99.76 Very High Very High Very High
Hypoglycemia 464 99.26 Very High Very High Very High
Alzheimer's Dementia 8 99.24 Very High Very High Very High
Insulin Resistance 256 98.88 Very High Very High Very High
Weight Loss 32 97.36 Very High Very High Very High
Obesity 160 96.44 Very High Very High Very High
Atherosclerosis 160 95.40 Very High Very High Very High
Hyperglycemia 176 93.64 High High
Targeted Disruption 44 91.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The sulfonylureas tolbutamide (100 micromol/l) and glibenclamide (100 nmol/l) inhibited glucagon secretion to the same extent as a maximally inhibitory concentration of glucose.
Negative_regulation (inhibited) of Localization (secretion) of glucagon
1) Confidence 0.53 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.06
Whereas insulin secretion increased monotonically with increasing external K+ concentrations (threshold 25 mmol/l), glucagon secretion was paradoxically suppressed at intermediate concentrations (5.6-15 mmol/l), and stimulation was first detectable at >25 mmol/l K+.
Negative_regulation (suppressed) of Localization (secretion) of glucagon in external
2) Confidence 0.53 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.15
In wild-type mouse islets, glucose produced a concentration-dependent (half-maximal inhibitory concentration [IC50]=2.5 mmol/l) reduction of glucagon release.
Negative_regulation (reduction) of Localization (release) of glucagon
3) Confidence 0.53 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.03
In mice lacking functional KATP channels (SUR1-/-), glucagon secretion in the absence of glucose was lower than that observed in wild-type islets and both glucose (0-20 mmol/l) and the sulfonylureas failed to inhibit glucagon secretion.
Negative_regulation (inhibit) of Localization (secretion) of glucagon
4) Confidence 0.53 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.08
Clonidine-displacing substance reduces glucagon secretion from mouse pancreatic alpha-cells by K(ATP)-channel-independent inhibition of exocytosis.
Negative_regulation (reduces) of Localization (secretion) of glucagon associated with clonidine
5) Confidence 0.49 Published 2001 Journal Biochem. Biophys. Res. Commun. Section Title Doc Link 11606044 Disease Relevance 0 Pain Relevance 0.20
Inhibition of glucagon release was not associated with a change in whole-cell ATP-sensitive K(+)-channel activity in single alpha-cells.
Negative_regulation (Inhibition) of Localization (release) of glucagon
6) Confidence 0.49 Published 2001 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 11606044 Disease Relevance 0 Pain Relevance 0.16
-Cell Specific Overexpression of Human Islet Amyloid Polypeptide

Exogenous administration of islet amyloid polypeptide (IAPP) has been shown to inhibit both insulin and glucagon secretion.

Negative_regulation (inhibit) of Localization (secretion) of glucagon associated with alzheimer's dementia
7) Confidence 0.37 Published 2008 Journal Experimental Diabetes Research Section Title Doc Link PMC2443691 Disease Relevance 0.46 Pain Relevance 0.14
administration of IAPP at supraphysiological doses inhibits glucagon secretion [8–11].
Negative_regulation (inhibits) of Localization (secretion) of glucagon
8) Confidence 0.37 Published 2008 Journal Experimental Diabetes Research Section Body Doc Link PMC2443691 Disease Relevance 0.27 Pain Relevance 0
CDS (5 U/ml) produced a 35% inhibition (P < 0.05) of glucagon release from intact islets.
Negative_regulation (inhibition) of Localization (release) of glucagon
9) Confidence 0.36 Published 2001 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 11606044 Disease Relevance 0 Pain Relevance 0.16
GLP-1 receptors have been identified in the pancreas (beta and alpha cells), kidney, heart, stomach, lung, and brain.8,9 GLP-1 enhances glucose-dependent insulin secretion, causes glucose-dependent suppression of elevated glucagon secretion, slows gastric emptying, and reduces food intake.
Negative_regulation (suppression) of Localization (secretion) of glucagon in lung
10) Confidence 0.18 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.61 Pain Relevance 0.04
The glucoregulatory mechanisms by which GLP-1 and exenatide/liraglutide act are similar, but GLP-1 suppresses gastric acid secretion, whereas exenatide and liraglutide do not.10 DPP-4 inhibitors augment insulin secretion and inhibit glucagon release, but do not slow gastric emptying and are weight neutral.11
Negative_regulation (inhibit) of Localization (release) of glucagon
11) Confidence 0.18 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.49 Pain Relevance 0.03
GLP-1 agonists (exenatide and liraglutide) and dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin, vildagliptin, and alogliptin) improve insulin secretion by pancreatic beta cells, and decrease the elevated rate of glucagon secretion by alpha cells.
Negative_regulation (decrease) of Localization (secretion) of glucagon in pancreatic beta cells associated with agonist
12) Confidence 0.18 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.69 Pain Relevance 0.05
The main physiologic role of glucagon is to oppose the action of insulin on HGP in order to protect against hypoglycemia and restore normoglycemia.111 GLP-1 inhibits the inappropriately high glucagon secretion after a meal, both directly through the GLP-1 receptor on the alpha cell and indirectly by stimulating insulin secretion, although the absolute contribution of each component is still debated.112 This glucose-dependent inhibitory effect of GLP-1 on glucagon secretion reduces HGP and decreases postprandial plasma glucose levels.113

Correction of accelerated gastric emptying

Negative_regulation (inhibits) of Localization (secretion) of glucagon in alpha cell associated with hypoglycemia
13) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.42 Pain Relevance 0
With regard to the beta cell defect, pioglitazone decreases lipotoxicity and exerts direct effects via the peroxisome-proliferator activated receptor-gamma to augment insulin secretion, while alogliptin improves islet function by increasing insulin secretion and lowering glucagon secretion in response to elevated plasma glucose levels.
Negative_regulation (lowering) of Localization (secretion) of glucagon in plasma
14) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.45 Pain Relevance 0.03
For over 30 years, it has been known that fasting plasma glucagon levels are increased in T2DM and that glucagon secretion is not appropriately suppressed following a carbohydrate or mixed meal or may paradoxically increase.105–107 This abnormality is evident before the diagnosis of diabetes, and has been observed in subjects with IGT.108–110 Hyperglucagonemia in the fasting state results in excessive HGP and elevated FPG levels, while impaired suppression of plasma glucagon levels following a meal results in postprandial hyperglycemia.
Neg (not) Negative_regulation (suppressed) of Localization (secretion) of glucagon in plasma associated with hyperglycemia and diabetes mellitus
15) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.57 Pain Relevance 0
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.
Negative_regulation (inhibiting) of Localization (secretion) of glucagon in neural
16) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.39 Pain Relevance 0.03
The greater reduction in postprandial glucose excursion with exenatide was accounted for by a higher insulinogenic index, a greater inhibition of glucagon secretion, and delayed gastric emptying.
Negative_regulation (inhibition) of Localization (secretion) of glucagon associated with gastric motility disorder
17) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.23 Pain Relevance 0.16
Glucagon-like peptide-1 deficiency/resistance contributes to islet cell dysfunction by impairing insulin secretion and increasing glucagon secretion.
Negative_regulation (impairing) of Localization (secretion) of glucagon
18) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Abstract Doc Link PMC2941781 Disease Relevance 0.70 Pain Relevance 0
However, unlike GLP-1, GIP does not inhibit glucagon secretion, does not slow gastric emptying, inhibit food intake, or promote weight loss.88 Both GLP-1 and GIP are rapid degraded by the DPP-4, which is ubiquitously present in plasma and on all cell membranes.
Negative_regulation (inhibit) of Localization (secretion) of glucagon in plasma associated with weight loss
19) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.47 Pain Relevance 0.04
plasma FFA), increased incretin effect, enhanced insulin secretion, and decreased glucagon secretion (Figure 10).
Negative_regulation (decreased) of Localization (secretion) of glucagon in plasma
20) Confidence 0.13 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.98 Pain Relevance 0

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