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)

Carbidopa, a selective extracerebral decarboxylase inhibitor, was given to 10 normal volunteers to determine its effects on endogenous catecholamine, indoleamine, and endocrine function. Tryptamine, which is largely extracerebral in origin, was inhibited markedly (80 percent) by the carbidopa; 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenolglycol (MHPG) excretion also were inhibited by the drug but not to the same degree as tryptamine. These differential results may be due partly to the higher central nervous system origin of the 5-HIAA and MHPG but also to a peripheral "stores" effect. In addition, carbidopa resulted in significant increases in plasma prolactin and a small but significant decrease in plasma glucagon.
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PMID:The effect of a peripheral decarboxylase inhibitor (carbidopa) on monoamine and neuroendocrine function in man. 55 49

The effects of an indoleamine, tryptamine, on plasma glucagon levels were investigated in mice. Tryptamine induced dose-related increases in plasma glucagon levels. The hyperglucagonemia effects of tryptamine were completely antagonized by methysergide and ketanserin which have a high affinity to 5-HT2 receptors. In addition, the peripheral 5-HT2 receptor antagonist, xylamidine, also strongly inhibited tryptamine-induced hyperglucagonemia. Our results indicate that the peripheral 5-HT2 receptors mediate the increase in plasma glucagon levels induced by tryptamine and that these receptors may have a role in the control of glucagon secretion.
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PMID:Hyperglucagonemia induced in mice by tryptamine: involvement of the peripheral 5-HT2 receptors. 139 14

Our previous study indicated that tryptamine induces a dose-related increase in plasma glucagon levels of mice and that this effect is mediated by the peripheral serotonin2 (5-HT2) receptor. The present paper further investigated the involvement of serotonergic and catecholaminergic systems in hyperglucagonemia elicited by tryptamine. An inhibitor of 5-HT synthesis, p-chlorophenylalanine, did not affect tryptamine-induced increases in plasma glucagon levels. Tryptamine-induced hyperglucagonemia was not inhibited by adrenalectomy or by an inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine. These findings indicate that tryptamine-induced hyperglucagonemia is elicited by its direct activation of 5-HT2 receptors and is not mediated by levels of endogenous 5-HT and catecholamines. The results further suggest that the peripheral 5-HT2 receptor has a possible role in the release of glucagon.
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PMID:Effects of tryptamine on plasma glucagon levels in mice. 790 28

Effects of tryptamine on tolbutamide-induced hypoglycemia were investigated in mice. Tryptamine significantly inhibited hypoglycemia elicited by tolbutamide. The inhibitory effects of tryptamine were strongly blocked by the 5-HT1 and 5-HT2 receptor antagonist methysergide and the 5-HT2 receptor antagonist ketanserin, while the 5-HT3 receptor antagonist ICS 205-930 was without effect. Tryptamine induced hyperglucagonemia in tolbutamide-treated mice, and this effect elicited by tryptamine was strongly inhibited by the 5-HT2 receptor antagonist ketanserin. These results suggest that the inhibitory effects of tryptamine on tolbutamide-induced hypoglycemia are mediated by 5-HT2 receptors and that tryptamine is involved in glucagon release.
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PMID:Inhibitory effects of tryptamine on tolbutamide-induced hypoglycemia in mice: mediation by 5-HT receptors. 813 57