消化管グルカゴン分泌動態に関する研究

抄録

Experiments have been carried out to determine whether a stimulatory effect of glucose administerd orally on the secretion of gut glucagon was associated with the absorption process of glucose from the intestine. For this purpose, oral and intravenous glucose tolerance tests were performed in gastrectomized subjects treated 60 minutes previously with phenformin (DBI) which has been reported to cause an impairment of intestinal absorption of glucose, and changes in blood sugar, IRI, total IRG and pancreatic glucagon levels were compared with those obtained during the control experiment in which no DBI was administered previously.
DBI pretreatment flattened the blood sugar and IRI responses to oral glucose significantly but did not alter the response to the intravenous glucose. The drug produced no significant changes in basal plasma pancreatic glucagon and total IRG levels. Thirty minutes after the oral glucose alone, the total IRG level rose to a peak of 1.55±0.17ng/ml, a value being not different from the maximum level of 1.67±0.18ng/ml observed during the test pretreated with DBI. However, the mean total IRG levels obtained 120 and 180 minutes after the oral glucose with DBI were significantly higher than the corresponding values without DBI which seemed to be attributed to glucose retention in the gut caused by the drug. No significant changes in mean plasma levels of pancreatic glucagon were noted after the oral glucose with and without DBI. The intravenous injection of glucose caused a slight decline in total IRG concentration to the same extent in the both occasions.
These results suggest that gut glucagon is released in response to contact of glucose with the intestinal mucosal surface rather than the intestinal absorption of glucose.