Effect of intrapancreatic administration of amino acids upon glucagon secretion in dogs.

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  • OHNEDA AKIRA
    Department of Internal Medicine, Tohoku University School of Medicine
  • ISHII SHOJI
    Department of Internal Medicine, Tohoku University School of Medicine
  • ITABASHI HIROSHI
    Department of Internal Medicine, Tohoku University School of Medicine
  • HORIGOME KEN
    Department of Internal Medicine, Tohoku University School of Medicine

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タイトル別名
  • Effect of Intrapancreatic Administratio

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説明

To see the direct effect of individual amino acids upon glucagon secretion, experiments were conducted, using in situ perfusion preparations of the canine pancreas. Twelve amino acids, alanine, arginine, glycine, leucine, histidine, isoleucine, lysine, methionine, phenylalanine, threonine, tryptophan and valine, were infused in a dose of 2. 3 mmoles over a 10-min period into the pancreatic artery of a group of 4 to 7 dogs, and plasma glucagon (IRG) and insulin (IRI) in the pancreatic vein were determined. After the infusion of the individual amino acids, blood glucose in the femoral artery did not change at all. Although the amino acids stimulated the insulin secretion, there were differences between the amino acids in the pattern of IRI response and in the IRI stimulating activity. The individual amino acids caused different responses of plasma IRG. The administration of arginine and threonine resulted in a remarkable rise of IRG, whereas leucine, tryptophan, isoleucine or lysine failed to enhance plasma IRG. Although there was no significant correlation between the increment areas of IRI and IRG, potency of the amino acids to stimulate both insulin and glucagon was roughly parallel. The results of the present experiment indicate that there are differences in a glucagon-stimulating activity of the individual amino acids, among which arginine and threonine are most potent. Furthermore, discrepancy observed in the enhancement of both IRI and IRG suggests the complicated mechanism in the secretion of islet hormones and does not support the intrainsular interaction of insulin and glucagon.

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