INT77415

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Context Info
Confidence 0.63
First Reported 1998
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 23
Total Number 24
Disease Relevance 11.10
Pain Relevance 1.69

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

small molecule metabolic process (GLP1R) plasma membrane (GLP1R) signal transducer activity (GLP1R)
Anatomy Link Frequency
small intestine 3
plasma 2
gut 1
neural 1
blood 1
GLP1R (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 100 100.00 Very High Very High Very High
tolerance 36 98.40 Very High Very High Very High
bradykinin 7 98.22 Very High Very High Very High
substance P 7 97.74 Very High Very High Very High
Enkephalin 1 97.48 Very High Very High Very High
Neuropeptide 25 91.52 High High
adenocard 18 83.84 Quite High
potassium channel 12 80.40 Quite High
intrathecal 1 76.40 Quite High
Paracetamol 2 45.68 Quite Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 940 99.92 Very High Very High Very High
Disease Progression 25 99.32 Very High Very High Very High
Brain Injury 1 99.28 Very High Very High Very High
Impaired Glucose Tolerance 36 98.72 Very High Very High Very High
Natriuresis 5 98.68 Very High Very High Very High
Obesity 83 96.20 Very High Very High Very High
Insulin Resistance 54 92.88 High High
Sprains And Strains 4 91.52 High High
Hypoglycemia 143 91.28 High High
Apoptosis 11 88.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In order to utilise GLP-1 action for type 2 diabetes therapy, two options are presently available [6]:
Localization (action) of GLP-1 associated with diabetes mellitus
1) Confidence 0.63 Published 2010 Journal Pediatr Nephrol Section Body Doc Link PMC2874027 Disease Relevance 0.60 Pain Relevance 0.17
GLP-1-receptor agonists (or GLP-1 mimetics) as injectable compoundsDipeptidyl-peptidase-IV (DPP-4) inhibitors (or incretin enhancers) as orally active substances
Localization (mimetics) of GLP-1 associated with agonist
2) Confidence 0.63 Published 2010 Journal Pediatr Nephrol Section Body Doc Link PMC2874027 Disease Relevance 0.59 Pain Relevance 0.16
GLP-1-receptor agonists (or GLP-1 mimetics) as injectable compoundsDipeptidyl-peptidase-IV (DPP-4) inhibitors (or incretin enhancers) as orally active substances
Localization (mimetics) of GLP-1-receptor associated with agonist
3) Confidence 0.63 Published 2010 Journal Pediatr Nephrol Section Body Doc Link PMC2874027 Disease Relevance 0.64 Pain Relevance 0.16
Neutral endopeptidase (NEP) is the major enzyme involved in the metabolic inactivation of a number of bioactive peptides including the enkephalins, substance P, endothelin, bradykinin and atrial natriuretic factor, as well as the incretin hormone glucagon-like peptide 1 (GLP-1), which is a potent stimulator of insulin secretion.
Localization (secretion) of GLP-1 associated with natriuresis, enkephalin, bradykinin and substance p
4) Confidence 0.63 Published 2007 Journal Acta Crystallogr. D Biol. Crystallogr. Section Abstract Doc Link 17704566 Disease Relevance 0.26 Pain Relevance 0.20
The incretin hormones GLP-1 and GIP (gastric inhibitory polypeptide, later often also referred to as glucose insulinotropic polypeptide) are secreted postprandially from the endocrine L- and K-cells in the intestinal mucosa respectively.
Localization (secreted) of GLP-1
5) Confidence 0.59 Published 2010 Journal Pediatr Nephrol Section Body Doc Link PMC2874027 Disease Relevance 0.40 Pain Relevance 0.05
Role of saxagliptin as monotherapy or adjunct therapy in the treatment of type 2 diabetes

Type 2 diabetes is associated with decreased incretin hormone response to an oral glucose load, and a progressive decline in postprandial glucagon-like peptide-1 (GLP-1) secretion.

Localization (secretion) of GLP-1 associated with diabetes mellitus
6) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Title Doc Link PMC2878957 Disease Relevance 0.29 Pain Relevance 0
Incretin hormone glucose-dependent insulinotropic peptide (GIP) is mainly secreted by the K cells in the duodenum and the proximal small intestine and glucagon-like peptide-1 (GLP-1) is secreted from the L cells of the distal gut.
Localization (secreted) of GLP-1 in small intestine
7) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2878957 Disease Relevance 0.91 Pain Relevance 0.10
Some studies have demonstrated a progressive decline in postprandial GLP-1 secretion, where individuals with normal glucose tolerance secrete more than those with impaired glucose tolerance, and individuals with type 2 diabetes demonstrate the greatest impairment in GLP-1 secretion.11 The clinical utility of native GLP-1 is limited by its short half-life (<2 minutes) due to its rapid degradation to inactive metabolites by the enzyme dipeptidyl peptidase-4 (DPP-4).10 Because of this limitation, new treatment approach has been developed to inhibit DPP-4 enzyme and thereby increase endogenous incretin hormone levels.
Localization (secretion) of GLP-1 associated with diabetes mellitus, tolerance and impaired glucose tolerance
8) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2878957 Disease Relevance 0.56 Pain Relevance 0.10
Incretin hormone glucose-dependent insulinotropic peptide (GIP) is mainly secreted by the K cells in the duodenum and the proximal small intestine and glucagon-like peptide-1 (GLP-1) is secreted from the L cells of the distal gut.
Localization (secreted) of glucagon-like peptide-1 in small intestine
9) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2878957 Disease Relevance 0.93 Pain Relevance 0.10
Role of saxagliptin as monotherapy or adjunct therapy in the treatment of type 2 diabetes

Type 2 diabetes is associated with decreased incretin hormone response to an oral glucose load, and a progressive decline in postprandial glucagon-like peptide-1 (GLP-1) secretion.

Localization (secretion) of glucagon-like peptide-1 associated with diabetes mellitus
10) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Title Doc Link PMC2878957 Disease Relevance 0.29 Pain Relevance 0
Specifically, it has been demonstrated that the endogenous human incretin hormone GLP-1 decreases blood glucose by several pathways – via the regulation of insulin and glucagon, inhibition of gastric emptying, and suppression of appetite, and that the normal physiologic response to GLP-1 is impaired in type 2 diabetes.9,10,11 GLP-1 stimulates insulin secretion in a glucose-dependent manner and suppresses glucagon secretion.10 In normal physiology, oral ingestion of nutrients stimulates GIP and GLP-1 secretion, which in turn increases insulin secretion from pancreatic beta-cells.
Localization (secretion) of GLP-1 in blood associated with diabetes mellitus
11) Confidence 0.55 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2878957 Disease Relevance 0.59 Pain Relevance 0.08
Clearance of native GLP-1 and its metabolites is largely mediated via the kidneys [5].
Localization (Clearance) of GLP-1
12) Confidence 0.53 Published 2010 Journal British Journal of Clinical Pharmacology Section Body Doc Link PMC2997321 Disease Relevance 0.46 Pain Relevance 0
Native GLP-1 is, however, rapidly metabolized by enzymes such as dipeptidyl peptidase-IV (DPP-IV), giving it a very short half-life (t1/2 < 2 min) [5, 15] and limiting its potential to be deployed as a therapeutic agent [10].
Localization (metabolized) of GLP-1
13) Confidence 0.53 Published 2010 Journal British Journal of Clinical Pharmacology Section Body Doc Link PMC2997321 Disease Relevance 0.94 Pain Relevance 0
Plasma concentrations of both incretins increase within 5 to 15 min after meal ingestion: GLP-1 is primarily released by the ingestion of carbohydrate, fat and protein, whereas GIP is mainly liberated by the ingestion of carbohydrate and fat (Deacon 2005).
Localization (released) of GLP-1 in Plasma
14) Confidence 0.50 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.31 Pain Relevance 0.08
Theoretically, DPP-4 inhibition seems to have the strongest potential in early stages of type 2 diabetes because of the impaired GLP-1 secretion in type 2 diabetes, together with both poor insulin secretion and sensitivity as well as partial insensitivity to GLP-1.
Localization (secretion) of GLP-1 associated with diabetes mellitus
15) Confidence 0.50 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.66 Pain Relevance 0
Almost 50% of this degradation occurs at the intestinal capillaries close to the site of GLP-1 and GIP release.
Localization (release) of GLP-1
16) Confidence 0.50 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.31 Pain Relevance 0
-cells, GLP-1 may also promote insulin secretion indirectly through the activation of sensory nerves (Ahrén 2004) suggesting an important neural contribution to GLP-1-induced insulin secretion, which could explain the rapid insulinotropic action after meal ingestion (Holst and Deacon 2005).
Localization (secretion) of GLP-1-induced in neural
17) Confidence 0.50 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.22 Pain Relevance 0.14
GLP-1 is a 30 amino acid polypeptide, which is produced by the intestinal L-cells localized mainly in the distal portion of the small intestine and in the large intestine.
Localization (localized) of GLP-1 in large intestine
18) Confidence 0.47 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.33 Pain Relevance 0
-cells, GLP-1 may also promote insulin secretion indirectly through the activation of sensory nerves (Ahrén 2004) suggesting an important neural contribution to GLP-1-induced insulin secretion, which could explain the rapid insulinotropic action after meal ingestion (Holst and Deacon 2005).
Localization (secretion) of GLP-1 in sensory nerves
19) Confidence 0.44 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2597770 Disease Relevance 0.16 Pain Relevance 0.15
The gut peptide glucagon-like peptide 1(7-36) amide (GLP-1) is released into the circulation after food intake.
Localization (released) of glucagon-like peptide 1 in gut
20) Confidence 0.31 Published 1998 Journal Am. J. Clin. Nutr. Section Abstract Doc Link 9734726 Disease Relevance 0.22 Pain Relevance 0

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