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Gastric A-cell function in normal dogs

L Muñoz-Barragan, E Blazquez, G S Patton

    The American Journal of Physiology
    |October 1, 1976
    PubMed
    Summary
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    In normal dogs, the gastric fundus is not a major source of circulating glucagon. Pancreatic glucagon release is significantly higher, especially after arginine stimulation.

    Area of Science:

    • Endocrinology
    • Gastroenterology
    • Metabolic Research

    Background:

    • Glucagon is a key hormone regulating blood glucose levels.
    • The primary source of glucagon is traditionally considered the pancreas.
    • The potential contribution of the gastric fundus to circulating glucagon requires further investigation.

    Purpose of the Study:

    • To compare glucagon release from the gastric fundus versus the pancreas in normal dogs.
    • To determine if the gastric fundus contributes significantly to circulating glucagon levels under various physiological conditions.

    Main Methods:

    • Measurement of plasma glucagon concentrations in major gastroepiploic, superior pancreaticoduodenal, and inferior vena cava veins in dogs.
    • Analysis of glucagon levels in basal states and following intravenous arginine infusion.

    Related Experiment Videos

  • Assessment of glucagon response to intragastric arginine, insulin-induced hypoglycemia, and phloridzin-induced hypoglycemia.

    • Main Results:

    • Basal glucagon levels in the gastric vein were not significantly different from the vena cava.
    • Pancreaticoduodenal vein glucagon levels were significantly higher than in the vena cava.
    • Arginine infusion caused a modest, transient increase in gastric vein glucagon, but a much larger increase in pancreatic vein glucagon.

    Conclusions:

    • The gastric fundus is not a major source of circulating glucagon in normal dogs under the studied conditions.
    • The pancreas is the predominant source of glucagon, particularly in response to stimuli like arginine.
    • Further research may explore specific conditions or alternative pathways for gastric glucagon secretion.