Abstract
In order to elucidate the role of glucagon in abnormal glucose tolerance after gastrectomy, we performed total gastrectomy in male Wistar rats using Billroth's 1st method, and the plasma glucagon levels after oral glucose loading in 15 gastrectomized rats were determined. As controls, 14 normal rats and 9 rats with a duodenal pouch (a catheter was inserted into the intraduodenum) were also investigated.
In the present experiments, after overnight fasting, the bilateral jugular veins were exposed under anesthesia with chloral hydrate (300mg/kg, intraperitoneally), and blood sampling was carried out with a heparinized syringe at intervals up to 90 min. All subjects were given 2g/kg of glucose (50% solution) orally through a polyethyelene catheter which was inserted into the stomach.
Blood glucose was determined by the orthotoluidine method and plasma insulin by polyethyleneglycol radioimmunoassay using rat insulin as standard. Plasma glucagon (IRG) was measured by the talcum method using antiserum 30 K, and plasma total glucagon (GLI) was determined by the same method using antiserum K 4023.
The blood glucose levels in the gastrectomized group after glucose loading were significantly elevated compared to those in noraml rats and the rats with a duodenal pouch.
The fasting plasma GLI level in the gastrectomized rats was 705±138.5 pg/ml, which was significantly higher than those in normal rats and the rats with a duodenal pouch (P<0.02 and P<0.05, respectively). The plasma GLI response to oral glucose loading in the gastrectomized rats was significantly higher than those in the other tow gourps (P<0.02). The fasting IRG level in the gastrectomized rats was also elevated compared to those in the other two groups. The plasma IRG levels following oral glucose administration rose abruptly to 785±233.0 pg/ml at 15 min after glucose loading. This level was also significantly higher than those in the other two groups (P<0.01).
No significant difference in plasma insulin response to glucose was observed among the three groups.
These results suggest that the IRG and GLI levels in gastrectomized rats may be elevated by a certain mechanism other than rapid passage through the intestine of glucose, and the elevated IRG may contribute to the glucose intolerance observed in gastrectomized rats.
