Gastric inhibitory polypeptide (GIP) in chronic pancreatitis.

Abstract

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.

• Authors: J L Botha, A I Vinik, J C Brown
• Journal: The Journal of clinical endocrinology and metabolism (J Clin Endocrinol Metab) Vol. 42 Issue 5 Pg. 791-7 (May 1976) ISSN: 0021-972X [Print] United States
• PMID: 1270574 (Publication Type: Journal Article)

Chemical References

• Antigens
• Blood Glucose
• Insulin
• Peptides
• Glucagon
• Glucose

Topics

• Adult
• Aged
• Antigens
• Blood Glucose (analysis, metabolism)
• Chronic Disease
• Digestive System (drug effects, metabolism)
• Fasting
• Glucagon (blood)
• Glucose (pharmacology)
• Glucose Tolerance Test
• Humans
• Insulin (blood)
• Male
• Middle Aged
• Pancreas (drug effects)
• Pancreatitis (blood)
• Peptides (blood, metabolism)