INT2275

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Context Info
Confidence 0.59
First Reported 1975
Last Reported 2010
Negated 3
Speculated 6
Reported most in Abstract
Documents 183
Total Number 195
Disease Relevance 51.02
Pain Relevance 44.94

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 (Ins1) extracellular region (Ins1) carbohydrate metabolic process (Ins1)
cytoplasm (Ins1)
Anatomy Link Frequency
pancreatic islets 20
pancreas 16
B cells 6
beta cell 6
plasma 4
Ins1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Clonidine 196 100.00 Very High Very High Very High
agonist 175 100.00 Very High Very High Very High
tolerance 160 100.00 Very High Very High Very High
anesthesia 62 100.00 Very High Very High Very High
narcan 50 100.00 Very High Very High Very High
Somatostatin 48 100.00 Very High Very High Very High
Catecholamine 29 100.00 Very High Very High Very High
Bile 15 100.00 Very High Very High Very High
qutenza 22 99.84 Very High Very High Very High
Dynorphin 29 99.82 Very High Very High Very High
Disease Link Frequency Relevance Heat
Diabetes Mellitus 1412 100.00 Very High Very High Very High
Impaired Glucose Tolerance 176 100.00 Very High Very High Very High
Obesity 144 100.00 Very High Very High Very High
Hyperinsulinism 76 100.00 Very High Very High Very High
Stress 70 100.00 Very High Very High Very High
Pressure And Volume Under Development 44 100.00 Very High Very High Very High
Urological Neuroanatomy 16 99.98 Very High Very High Very High
Insulin Resistance 217 99.90 Very High Very High Very High
Hyperglycemia 121 99.90 Very High Very High Very High
Bordatella Infection 23 99.86 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We conclude that immediately after hepatic dearterialization in rats with liver malignancies, glucose intolerance and impaired glucose-induced insulin secretion exist.
Negative_regulation (impaired) of Localization (secretion) of insulin in liver associated with impaired glucose tolerance
1) Confidence 0.59 Published 1989 Journal J. Surg. Res. Section Abstract Doc Link 2666752 Disease Relevance 0.48 Pain Relevance 0.06
We conclude that the activation of preoptic alpha2-adrenoceptors induced hyperglycemia and inhibit insulin secretion, probably by activation of the sympathoadrenal system that cannot be blocked by prior administration of guanethidine.
Negative_regulation (inhibit) of Localization (secretion) of insulin associated with hyperglycemia and guanethidine
2) Confidence 0.58 Published 2003 Journal Brain Res. Section Abstract Doc Link 12957368 Disease Relevance 0.45 Pain Relevance 0.42
The inhibition of 86Rb+ efflux persisted when insulin release was prevented by omission of extracellular calcium.
Negative_regulation (prevented) of Localization (release) of insulin
3) Confidence 0.58 Published 1983 Journal Am. J. Physiol. Section Abstract Doc Link 6338738 Disease Relevance 0 Pain Relevance 0.14
Epinephrine abolished insulin release but inhibited 45Ca2+ efflux only partially during stimulation by glucose or by barium plus theophylline.
Negative_regulation (abolished) of Localization (release) of insulin
4) Confidence 0.58 Published 1983 Journal Am. J. Physiol. Section Abstract Doc Link 6338738 Disease Relevance 0 Pain Relevance 0.12
These results support the interpretation that chronic sucrose ingestion inhibits pancreatic insulin secretion and elevates blood pressure by stimulating the ventromedial hypothalamus to increase sympathetic activity.
Negative_regulation (inhibits) of Localization (secretion) of insulin in hypothalamus
5) Confidence 0.58 Published 1983 Journal Hypertension Section Abstract Doc Link 6337950 Disease Relevance 0.31 Pain Relevance 0.12
A-18-F-amide (10, 100, 1000 pM) inhibited concentration dependently glucose (10 mM)- and arginine (10 mM)-induced insulin secretion from the isolated perfused rat pancreas during the first (controls: 100%; 10 pM: 114%; 100 pM: 63%, p less than 0.05; 1000 pM: 31%, p less than 0.05) and the second secretion phase (controls: 100%; 10 pM: 102%; 100 pM: 78%; 1000 pM: 27%, p less than 0.05).
Negative_regulation (inhibited) of Localization (secretion) of insulin in pancreas
6) Confidence 0.58 Published 1990 Journal Neuropeptides Section Abstract Doc Link 1704109 Disease Relevance 0 Pain Relevance 0.07
The opiate antagonist naltrexone decreases glucose-stimulated insulin release, while the sensitivity of diabetic rats to naloxone-induced satiety is increased.
Negative_regulation (decreases) of Localization (release) of insulin associated with diabetes mellitus, antagonist, narcan and opiate
7) Confidence 0.58 Published 1986 Journal Physiol. Behav. Section Abstract Doc Link 2947253 Disease Relevance 0.44 Pain Relevance 0.53
The inhibitory effect of lithium was counteracted by pretreatment of the rats with the alpha-adrenergic blocking agent dihydroergotamine, whereas the opiate antagonist naloxone had no apparent effect on lithium-induced inhibition of glucose-stimulated insulin release.
Negative_regulation (inhibition) of Localization (release) of insulin associated with antagonist, narcan and opiate
8) Confidence 0.58 Published 1987 Journal Diabetologia Section Abstract Doc Link 3556290 Disease Relevance 0 Pain Relevance 0.24
The results show that epinephrine does not inhibit insulin release by activating the Na pump or by increasing K permeability of the B cell membrane.
Negative_regulation (inhibit) of Localization (release) of insulin in B cell
9) Confidence 0.58 Published 1983 Journal Am. J. Physiol. Section Abstract Doc Link 6338738 Disease Relevance 0 Pain Relevance 0.11
These peptides (3.95 X 10(-8) M), like morphine (3.95 X 10(-8) M), significantly inhibited the glucose-induced insulin secretion.
Negative_regulation (inhibited) of Localization (secretion) of insulin associated with morphine
10) Confidence 0.58 Published 1986 Journal Tohoku J. Exp. Med. Section Abstract Doc Link 2877510 Disease Relevance 0 Pain Relevance 0.47
In order to settle the question about whether or not opioid peptides stimulate or inhibit insulin secretion, we studied effects of rimorphin and dynorphin, two members of the preproenkephalin B group, on glucose-induced insulin secretion in the isolated, perfused rat pancreas.
Spec (whether) Negative_regulation (inhibit) of Localization (secretion) of insulin in pancreas associated with dynorphin and opioid
11) Confidence 0.58 Published 1986 Journal Tohoku J. Exp. Med. Section Abstract Doc Link 2877510 Disease Relevance 0 Pain Relevance 0.36
The inhibitory effect of rimorphin was attenuated by naloxone (1.2 X 10(-6) M) and phentolamine (10(-6) M), suggesting an involvement of adrenergic alpha receptors in the inhibition of glucose-induced insulin secretion mediated through specific opiate receptors.
Negative_regulation (inhibition) of Localization (secretion) of insulin associated with narcan and opiate
12) Confidence 0.58 Published 1986 Journal Tohoku J. Exp. Med. Section Abstract Doc Link 2877510 Disease Relevance 0 Pain Relevance 0.48
Lithium (5 mmol/l) added 30 min prior to glucose stimulation or together with glucose (16.7 mmol/l) failed to affect first phase, but reduced second phase glucose-induced insulin release by 35%.
Neg (failed) Negative_regulation (reduced) of Localization (release) of insulin
13) Confidence 0.58 Published 1987 Journal Diabetologia Section Abstract Doc Link 3556290 Disease Relevance 0 Pain Relevance 0.19
The results suggest that the interaction of secreted endorphins with the sympathetic nervous system is the likely cause of the hyperglycaemia and the inhibition of the glucose-stimulated insulin release induced by lithium.
Negative_regulation (inhibition) of Localization (release) of insulin in sympathetic nervous system
14) Confidence 0.58 Published 1986 Journal Acta Endocrinol. Section Abstract Doc Link 2870599 Disease Relevance 0.17 Pain Relevance 0.28
Dihydroergotamine, but not naloxone, counteracts lithium as an inhibitor of glucose-induced insulin release in isolated rat islets in vitro.
Negative_regulation (inhibitor) of Localization (release) of insulin associated with narcan
15) Confidence 0.58 Published 1987 Journal Diabetologia Section Title Doc Link 3556290 Disease Relevance 0 Pain Relevance 0.25
In conclusion our results show that adrenergic inhibition of insulin secretion is mediated only by alpha 2-receptors whereas both types of adrenoceptors are implicated in the vasoconstrictor effect.
Negative_regulation (inhibition) of Localization (secretion) of insulin
16) Confidence 0.58 Published 1985 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2866972 Disease Relevance 0 Pain Relevance 0.46
An alpha 2-adrenoceptor agonist, clonidine 0.01 and 0.05 microM decreased insulin secretion (-80%).
Negative_regulation (decreased) of Localization (secretion) of insulin associated with agonist and clonidine
17) Confidence 0.58 Published 1985 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2866972 Disease Relevance 0 Pain Relevance 0.48
These data taken together with findings in previously reported work suggest that diltiazem reduces insulin secretion from pancreatic B-cells in vitro possibly by the calcium-antagonistic property, while the compound exhibits practically no inhibitory action on the insulin secretion in vivo.
Spec (possibly) Negative_regulation (reduces) of Localization (secretion) of insulin in B-cells
18) Confidence 0.58 Published 1979 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 395348 Disease Relevance 0 Pain Relevance 0
In the perfused rat pancreas, diltiazem reduced both glucose- and tolbutamide-induced insulin secretion and these effects of diltiazem were reversed with removal of the compound.
Negative_regulation (reduced) of Localization (secretion) of insulin in pancreas
19) Confidence 0.58 Published 1979 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 395348 Disease Relevance 0 Pain Relevance 0
Inhibition of the glucose-induced insulin secretion caused by diltiazem was counteracted by increasing the concentration of calcium ion.
Negative_regulation (Inhibition) of Localization (secretion) of insulin
20) Confidence 0.58 Published 1979 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 395348 Disease Relevance 0 Pain Relevance 0

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