Gastric Inhibitory Polypeptide (GIP) in Chronic Pancreatitis

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Abstract
The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI),andgutglucagon-likeimmunoreactivity (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 unimpaired 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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