INT280037

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Context Info
Confidence 0.25
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 4
Disease Relevance 2.22
Pain Relevance 0.13

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

cytoplasm (Gip)
Anatomy Link Frequency
beta cell 1
small intestine 1
Gip (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 23 97.26 Very High Very High Very High
agonist 45 27.36 Quite Low
Inflammation 15 5.00 Very Low Very Low Very Low
pruritus 6 5.00 Very Low Very Low Very Low
headache 6 5.00 Very Low Very Low Very Low
cytokine 5 5.00 Very Low Very Low Very Low
Neuropeptide 4 5.00 Very Low Very Low Very Low
abdominal pain 4 5.00 Very Low Very Low Very Low
Paracetamol 4 5.00 Very Low Very Low Very Low
substance P 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 388 99.90 Very High Very High Very High
Impaired Glucose Tolerance 20 97.26 Very High Very High Very High
Weight Loss 20 94.68 High High
Hypoglycemia 117 60.32 Quite High
Cardiovascular Disease 11 58.40 Quite High
Injury 3 14.00 Low Low
Apoptosis 4 11.76 Low Low
Bone Fracture 6 6.48 Low Low
Insulin Resistance 51 5.00 Very Low Very Low Very Low
Hyperglycemia 41 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In T2DM patients during hyperglycemic clamp studies, infusion of GLP-1, but not GIP, stimulates insulin secretion,19 establishing that the insulinotropic effect of GLP-1 is relatively well-preserved in T2DM, despite possibly lower levels, when compared to non-diabetic subjects.20 On the other hand, GIP levels are essentially normal in T2DM but GIP-stimulated second-phase insulin secretion is markedly diminshed21 (although it has recently been reported that reversal of poor glycemic control in T2DM improves the insulin response to both GIP and GLP-1).21 Hence, the development of incretin-based therapies for T2DM has hitherto focused on GLP-1, rather than GIP.
Localization (secretion) of GIP associated with diabetes mellitus
1) Confidence 0.25 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2731024 Disease Relevance 0.89 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 GIP
2) Confidence 0.24 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.47 Pain Relevance 0.05
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 GIP in beta cell associated with diabetes mellitus, tolerance and impaired glucose tolerance
3) Confidence 0.23 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.47 Pain Relevance 0.05
GIP is secreted by the K-cells of the early small intestine in response to meal ingestion.
Localization (secreted) of GIP in small intestine
4) Confidence 0.21 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 0.39 Pain Relevance 0.03

General Comments

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