Gastrointestinal Actions of Glucagon

Lin, T. M.

doi:10.1507/endocrj1954.27.supplement_87

Cited by 4 publications

(2 citation statements)

References 34 publications

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“…This suggests that CCK stimulates the release of PP by act ing via CCK receptors. Since PP is known to affect gastric secretion and gastric emptying [30] it remains to be established what role, if any, PP plays in the action of CCK on gastric functions observed in this report.…”

Section: Discussionmentioning

confidence: 92%

Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Konturek¹,

Kwiecień²,

Obtulowicz³

et al. 1990

Digestion

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Cholecystokinin (CCK) is known to inhibit gastric acid secretion and gastric emptying but its physiological role in the inhibition of gastric functions is not settled. In this study performed on 16 young male subjects, gastric acid secretion and emptying rate were determined after intragastric administration of 8 % peptone meal alone or in combination with intravenous infusion of graded doses of CCK-8 (5–80 pmol/kg·h) or with addition of vegetable oil to meal without or with pretreatment with loxiglumide, a specific CCK antagonist. CCK-8 infusion at lower dose (5 pmol/kg·h) was ineffective but at higher doses (20–80 pmol/kg·h) it resulted in a significant reduction in acid output by 39 and 43 % and a decrease in gastric emptying from 54% to 40 and 22%, respectively. Pretreatment with loxiglumide abolished almost completely the inhibition of both gastric acid and gastric emptying by CCK-8. Fat added to peptone meal reduced gastric acid secretion by 42–65% and decreased gastric emptying to 24–32%. The pretreatment with loxiglumide tended to reduce fat-induced inhibition of gastric acid secretion and gastric emptying but the difference in the inhibition of gastric functions between the tests without and with loxiglumide was not significant. This study provides evidence that exogenous CCK administered at pharmacological doses is a potent inhibitor of gastric acid secretion and gastric emptying and probably acts via specific CCK receptors. In contrast, fat induces inhibition of gastric acid secretion and gastric emptying that cannot be fully attributed to hormonally acting CCK.

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Section: Discussionmentioning

confidence: 92%

Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Konturek¹,

Kwiecień²,

Obtulowicz³

et al. 1990

Digestion

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“…Early studies that assessed the effect of intravenous glucagon on esophageal motor function evaluated only the lower esophageal sphincter (LES) resting pressure [2,3]. These studies and others have demonstrated in humans and animals that, after a latency period of 30-60 sec postadministration of glucagon, a significant reduction in LES resting pressure is achieved [2][3][4][5][6][7][8]. The duration of action may last 4-15 min and is probably a dose-dependent phenomena [4].…”

mentioning

confidence: 99%

Effect of Doses of Glucagon Used to Treat Food Impaction on Esophageal Motor Function of Normal Subjects

et al. 1999

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We studied 10 normal subjects to determine the effect of doses of intravenous glucagon used to treat food impaction on esophageal motor function. With a multilumen assembly perfused by a low compliance pneumohydraulic infusion pump, esophageal manometry was performed during baseline and after randomized administration of 0. 25, 0.5, and 1 mg intravenous glucagon. Mean proximal and distal amplitudes of contraction, proximal and distal amplitude of contraction duration, lower esophageal sphincter (LES) resting pressure, percentage of LES relaxation, and glucagon-related side effects were evaluated. No effect on proximal amplitude of contraction and proximal or distal esophageal contraction duration was noted. Mean amplitude of contraction in the distal esophagus was further reduced with increased dosage of glucagon but did not achieve statistical significance. Mean LES resting pressure was significantly reduced after 0.25 mg (18.7 +/- 1.8 vs. 10.2 +/- 1.5 mmHg, p = 0.0001) and further reduced after 0.5 mg (5.9 +/- 1.2 mmHg, p = 0.0009). Mean LES relaxation was significantly reduced after 0. 25 mg (93.1 +/- 2.4% vs. 63.6 +/- 8.8%, p = 0.0031). The 1-mg dose versus the 0.5-mg did not provide further reduction in any LES function parameters. One subject experienced transient nausea after 0.5 mg, and 4 subjects experienced nausea after 1 mg glucagon. In conclusion, increased doses of glucagon further reduce mean distal esophageal amplitude of contraction. Although maximum reduction in mean LES resting pressure was achieved with 0.5 mg, it did not provide any potential therapeutic advantage over 0.25 mg glucagon. Nausea is a common, transient side effect predominantly affecting subjects treated with the 1-mg dose.

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Dissociation of the spasmolytic and metabolic effects of glucagon

Jørgensen

Weis

Diamant

1983

European Journal of Pharmacology

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Gastrointestinal Actions of Glucagon

Abstract: Glucagon (Bromer et al., 1957; Staub et al., 1953), the hyperglycemic-glycogenolytic hormone isolated from the islets of the pancreas has a broad spectrum of gastrointestinal actions.

Cited by 4 publications

References 34 publications

Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Effect of Doses of Glucagon Used to Treat Food Impaction on Esophageal Motor Function of Normal Subjects

Dissociation of the spasmolytic and metabolic effects of glucagon

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