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Increased insulin resistance and β cell activity in patients with Crohn's disease
Background: Pancreatitis and exocrine pancreatitic insufficiency have been described as extraintestinal manifestations of inflammatory bowel disease. In this study, we investigated whether the endocrine pancreatic function is also disturbed in patients with inflammatory bowel disease. Methods: Seven...
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Published in: | Inflammatory bowel diseases 2006-01, Vol.12 (1), p.53-56 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background: Pancreatitis and exocrine pancreatitic insufficiency have been described as extraintestinal manifestations of inflammatory bowel disease. In this study, we investigated whether the endocrine pancreatic function is also disturbed in patients with inflammatory bowel disease.
Methods: Seventeen patients with Crohn's disease and 13 healthy volunteers participated in the study. We analyzed the plasma insulin response in a 75‐g oral glucose tolerance test. Glucose and insulin levels were determined at time 0 (fasting levels) and 30, 60, 90, 120, 180, 240, and 300 min after glucose uptake. Insulin resistance and β cell function (BCF) were analyzed by calculating respective indices.
Results: Fasting and oral glucose‐tolerance test glucose levels appeared to be similar in patients with Crohn's disease and in the controls. Impaired fasting glucose, impaired glucose tolerance, and/or overt diabetes mellitus were not observed in the volunteers. Insulin as well as the index for BCF were significantly increased in patients with Crohn's disease. In addition, insulin resistance was shown to be significantly elevated in Crohn's disease.
Conclusions: Patients with Crohn's disease reveal an increased insulin secretion caused by an enhanced BCF, which may be induced by an up‐regulated enteropancreatic axis. This hypersecretion may override the insulin resistance given by the chronic inflammatory state. |
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ISSN: | 1078-0998 1536-4844 |
DOI: | 10.1097/01.MIB.0000195975.97673.f5 |