Peculiar glucagon processing in the intestine is the genesis of the paradoxical rise of serum pancreatic glucagon in patients after total pancreatectomy.

BACKGROUND/AIMS Although glucagon has been detected even in the serum of totally pancreatectomized patients and the origin was suggested to be the intestine, the kinetics of glucagon are not well known after pancreatectomy. In the present study, we investigated the kinetics of glucagon and glucagon-related peptides in pancreatectomy patients and discuss the glucagon processes. METHODOLOGY Ten patients who had undergone total pancreatoduodenectomy reconstruction using Billroth II type procedures (group PX) and 12 normal subjects (group C) were also enrolled in this study. All patients received a 75-g oral glucose tolerance test in the early morning fasting state. Serum glucagon levels were assessed using the glucagon specific C-terminal (immunoreactive glucagon: IRG) and nonspecific N-terminal (glucagon-like immunoreactivity: GLI) radioimmunoassays. The molecular forms of these glucagon-related peptides were also estimated using the gel filtration chromatography method before and after the oral glucose load. RESULTS After the glucose load, serum GLIs were increased significantly in group PX suggesting that these were affected by the alimentary tract reconstructions. Serum IRGs were significantly increased in group PX, but decreased in group C after oral glucose load suggesting that these paradoxical increased responses in group PX might be associated with the insulin secretion deficiencies, but not associated with the alimentary tract reconstruction. CONCLUSIONS The paradoxical rise in IRGs based on the findings of gel filtration chromatography in group PX were possibly due to the generated peculiar glicentin-like peptide from the glucagon precursor, preproglucagon, after total pancreatectomy, which might be processed in intestines in association with the insulin deficiencies.