INT8740

Context Info Confidence 0.78 First Reported 1980 Last Reported 2011 Negated 0 Speculated 0 Reported most in Abstract Documents 65 Total Number 72 Disease Relevance 19.00 Pain Relevance 9.81

extracellular space (Gcg) extracellular region (Gcg) cytoplasm (Gcg)

Anatomy Link Frequency plasma 8 blood 5 alpha cell 4 pancreatic islets 3 skeletal muscles 2 Gcg (Mus musculus)

Pain Link Frequency Relevance Heat Somatostatin 31 99.40 Clonidine 20 99.40 qutenza 26 98.58 antagonist 172 98.20 member 8 7 98.08 Neuropeptide 24 97.58 Paracetamol 162 97.20 agonist 213 95.64 Action potential 27 94.64 tolerance 154 93.12

Disease Link Frequency Relevance Heat Hypoglycemia 598 99.82 Diabetes Mellitus 1763 99.80 Hyperglycemia 224 99.80 Gastric Motility Disorder 18 99.76 Cancer 84 99.44 Targeted Disruption 764 99.10 Insulin Resistance 310 98.88 Alzheimer's Dementia 33 98.74 Weight Loss 39 97.36 Metastasis 16 97.04

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Involvement of alpha1 and beta-adrenoceptors in adrenaline stimulation of the glucagon-secreting mouse alpha-cell.

Localization (secreting) of glucagon

1) Confidence 0.78 Published 2004 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Title Doc Link 14727006 Disease Relevance 0 Pain Relevance 0.15

The results indicate that alpha1- and beta-adrenoceptors on the alpha-cells mediate adrenaline-stimulated glucagon secretion.

Localization (secretion) of glucagon

2) Confidence 0.78 Published 2004 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 14727006 Disease Relevance 0 Pain Relevance 0.22

Stimulation of glucagon release and inhibition of insulin secretion from the islets of Langerhans are important for the blood-glucose-elevating effect of adrenaline.

Localization (release) of glucagon in blood

3) Confidence 0.78 Published 2004 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 14727006 Disease Relevance 0 Pain Relevance 0

In the present study we investigated how adrenaline affects the cytoplasmic Ca2+ concentration, which controls glucagon secretion from the pancreatic alpha-cell.

Localization (secretion) of glucagon

4) Confidence 0.78 Published 2004 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 14727006 Disease Relevance 0 Pain Relevance 0.09

In controls, 2-DG stimulated insulin and glucagon secretion and induced hyperglycemia (P less than 0.01).

Localization (secretion) of glucagon associated with hyperglycemia

5) Confidence 0.75 Published 1992 Journal J. Auton. Nerv. Syst. Section Abstract Doc Link 1378463 Disease Relevance 0.10 Pain Relevance 0.76

Furthermore, capsaicin-sensitive sensory nerve fibers are partially involved in 2-DG-induced glucagon secretion and hyperglycemia, whereas sensory nerves are not involved in 2-DG-induced insulin secretion.

Localization (secretion) of glucagon in sensory nerves associated with hyperglycemia and qutenza

6) Confidence 0.75 Published 1992 Journal J. Auton. Nerv. Syst. Section Abstract Doc Link 1378463 Disease Relevance 0.18 Pain Relevance 0.78

Neonatal capsaicin-treatment in mice: effects on pancreatic peptidergic nerves and 2-deoxy-D-glucose-induced insulin and glucagon secretion.

Localization (secretion) of glucagon in nerves associated with qutenza

7) Confidence 0.75 Published 1992 Journal J. Auton. Nerv. Syst. Section Title Doc Link 1378463 Disease Relevance 0.07 Pain Relevance 0.82

Patch-clamp recordings and glucagon release measurements were combined to determine the role of plasma membrane ATP-sensitive K+ channels (KATP channels) in the control of glucagon secretion from mouse pancreatic alpha-cells.

Localization (release) of glucagon in plasma

8) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0

We conclude that the KATP channel is involved in the control of glucagon secretion by regulating the membrane potential in the alpha-cell in a way reminiscent of that previously documented in insulin-releasing beta-cells.

Localization (secretion) of glucagon

9) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.19

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.

Localization (secretion) of glucagon

10) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.07

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.

Localization (secretion) of glucagon

11) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.06

ATP-sensitive K+ channel-dependent regulation of glucagon release and electrical activity by glucose in wild-type and SUR1-/- mouse alpha-cells.

Localization (release) of glucagon

12) Confidence 0.73 Published 2004 Journal Diabetes Section Title Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.03

Patch-clamp recordings and glucagon release measurements were combined to determine the role of plasma membrane ATP-sensitive K+ channels (KATP channels) in the control of glucagon secretion from mouse pancreatic alpha-cells.

Localization (secretion) of glucagon in plasma

13) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0

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+.

Localization (secretion) of glucagon in external

14) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.14

In wild-type mouse islets, glucose produced a concentration-dependent (half-maximal inhibitory concentration [IC50]=2.5 mmol/l) reduction of glucagon release.

Localization (release) of glucagon

15) Confidence 0.73 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.

Localization (secretion) of glucagon

16) Confidence 0.73 Published 2004 Journal Diabetes Section Abstract Doc Link 15561909 Disease Relevance 0 Pain Relevance 0.08

-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.

Localization (secretion) of glucagon associated with alzheimer's dementia

17) Confidence 0.69 Published 2008 Journal Experimental Diabetes Research Section Title Doc Link PMC2443691 Disease Relevance 0.46 Pain Relevance 0.14

in view of the inhibitory influence of insulin on glucagon secretion.

Localization (secretion) of glucagon

18) Confidence 0.69 Published 2008 Journal Experimental Diabetes Research Section Body Doc Link PMC2443691 Disease Relevance 0.19 Pain Relevance 0.19

administration of IAPP at supraphysiological doses inhibits glucagon secretion [8–11].

Localization (secretion) of glucagon

19) Confidence 0.69 Published 2008 Journal Experimental Diabetes Research Section Body Doc Link PMC2443691 Disease Relevance 0.27 Pain Relevance 0

glucagon secretion [8–11].

Localization (secretion) of glucagon

20) Confidence 0.69 Published 2008 Journal Experimental Diabetes Research Section Body Doc Link PMC2443691 Disease Relevance 0.19 Pain Relevance 0.22

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