Abstract
Summary
Plasma immunoreactive glucagon (IRG) and immunoreactive insulin (IRI) were measured in 21 gastrectomized and 11 normal subjects during a 3 hr, 100 g oral glucose tolerance test. Plasma IRG and IRI responses to oral glucose (50 g), oral galactose (100 g), oral fructose (100 g), and to intravenous glucose (25 g) were also investigated in some individuals.
Although no difference in the fasting IRG concentration between the two groups was found, 30 min after ingesting 100 g of glucose, the plasma IRG concentration of the gastrectomized subjects was significantly higher than that of the normal subjects (3.19 ± 0.26 vs 1.15 ± 0.08 mμg/ml; p < .005).
In gastrectomized patients, oral glucose caused hyperglucagonemia, also a marked rise in plasma IRI; whereas intravenous glucose load caused only a moderate increase in plasma IRI, with no changes in IRG concentration.
In the gastrectomized patients, a 50 g oral glucose load caused a significantly smaller plasma IRG response than a 100 g glucose load. The increment in plasma IRG level following galactose was smaller than that following glucose in both groups. However, the peak value of plasma IRG was significantly higher in the gastrectomized subjects than in the normals. After oral fructose administration, the gastrectomized subjects showed a small, but significant, increase in plasma IRG concentration. Glucose was the most potent stimulus for plasma IRG; and fructose was the weakest of the three sugars tested orally.
These results suggest that glucagon, probably of gastrointestinal origin, is released in response to chemical, as well as mechanical or osmotic, stimuli. The physiologic significance of enteric IRG is discussed.
We thank Dr. Piero P. Foà for his advice. We are also very grateful for the technical help of Misses Hiroko Iida and Mikiko Kobayashi.
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