Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of bicuculline methiodide (BMI), a gamma-aminobutyric acid (GABA) receptor antagonist, on central nervous system regulation of blood glucose homeostasis was studied in fed rats. Injection of BMI (1-10 nmol) into the third ventricle was found to produce hepatic venous hyperglycemia in a dose-dependent manner. This change was associated with increased secretion of epinephrine and glucagon. The role of epinephrine in hyperglycemia was then studied in bilaterally adrenalectomized (ADX) rats injected with BMI. Plasma glucose concentration was found to increase in ADX rats although the level was approximately half that for intact rats and significantly higher than for controls. The increase in epinephrine and glucagon secretion seen in intact rats, but not in ADX rats, suggests BMI induced epinephrine release is responsible for the glucagon secretion. Three possible mechanisms are suggested to account for the rise in plasma glucose in the hepatic vein after injection of BMI: 1) that epinephrine is secreted by the adrenal medulla, 2) that epinephrine secretion stimulates glucagon secretion or 3) that there may be some direct innervation of the liver in rats.
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PMID:Bicuculline methiodide influences the central nervous system to produce hyperglycemia in rats. 798 75

We investigated 1) the effect of immobilization stress on glucose metabolism in rats after sham operation (SHAM), adrenomedullectomy (ADMX), and adrenalectomy (ADX); and 2) the effect of glucoregulatory hormone infusion on plasma glucose using untreated normal fasted and fed rats under unanesthetized conditions. In immobilization stress, the plasma glucose concentration increased only in the SHAM group during fasting, while under fed conditions, all three groups showed significant increases (SHAM > ADMX > ADX). Plasma glucagon and norepinephrine significantly increased in all groups; plasma epinephrine increased only in the SHAM group, and plasma corticosterone increased in SHAM and ADMX groups under both conditions. The hepatic glycogen content in all fed groups significantly decreased after immobilization stress, while a very low content before stress and an undetectable level after stress were observed in all fasted groups. Only epinephrine infusion increased plasma glucose during fasting, while epinephrine and glucagon infusion increased it under fed conditions. Corticosterone infusion did not change it under either condition. These results suggest that in the fasted condition, only epinephrine plays an essential role, while under fed conditions, glucagon and corticosterone as well as epinephrine also act as synergistic factors in stress-induced hyperglycemia.
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PMID:Glucoregulatory hormones in the immobilization stress-induced increase of plasma glucose in fasted and fed rats. 847 65

To determine if pancreatic sympathetic nerves can contribute to increased glucagon secretion during hypoglycemia, plasma glucagon and pancreatic glucagon secretion in situ were measured before and during insulin-induced hypoglycemia in three groups of halothane-anesthetized dogs. All dogs were bilaterally vagotomized to eliminate the input from pancreatic parasympathetic nerves. One group of dogs received only vagotomy (VAGX). A second group was vagotomized and adrenalectomized (VAGX + ADX). A third group received vagotomy, adrenalectomy, plus surgical denervation of the pancreas (VAGX + ADX + NERVX) to prevent activation of pancreatic sympathetic nerves. In dogs with VAGX only, hypoglycemia increased plasma epinephrine (Epi), pancreatic norepinephrine (NE) output (+320 +/- 140 pg/min, P < 0.05), arterial plasma glucagon (+28 +/- 12 pg/ml, P < 0.01), and pancreatic glucagon output (+1,470 +/- 370 pg/min, P < 0.01). The addition of ADX eliminated the increase of Epi but did not increase pancreatic NE output (+370 +/- 190 pg/min, P < 0.025), arterial plasma glucagon (+20 +/- 5 pg/ml, P < 0.01), or pancreatic glucagon output (+810 +/- 200 pg/min, P < 0.01). In contrast, the addition of pancreatic denervation eliminated the increase of pancreatic NE output (-20 +/- 40 pg/min, P < 0.05 vs. VAGX), the arterial glucagon (+1 +/- 2 pg/ml, P < 0.01 vs. VAGX), and pancreatic glucagon output responses (+210 +/- 280 pg/min, P < 0.025 vs. VAGX) to hypoglycemia. Thus activation of pancreatic sympathetic nerves can contribute to the increased glucagon secretion during severe insulin-induced hypoglycemia in dogs.
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PMID:Pancreatic sympathetic nerves contribute to increased glucagon secretion during severe hypoglycemia in dogs. 877 69


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