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Case-control study reveals exaggerated gastric inhibitory polypeptide secretion following oral glucose in chronic pancreatitis, suggesting an incretin mechanism maintaining oral insulin response.
The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.
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Botha et al. (1976) studied this question.
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