135
Views
18
CrossRef citations to date
0
Altmetric
Article

Enhanced glucose‐dependent glucagon‐like peptide‐1 and insulin secretion in Crohn patients with terminal ileum disease is unrelated to disease activity or ileal resection

, , , , , , , & show all
Pages 650-656 | Received 09 Sep 2003, Accepted 21 Jan 2004, Published online: 08 Jul 2009
 

Abstract

Background: Enhanced secretion of glucagon‐like peptide‐1 (GLP‐1) has been reported in patients with Crohn disease (CD). However, the correlation between the enteropancreatic axis and the activity of CD remains unclear. Methods: Plasma glucose, insulin, GLP‐1 levels and insulin sensitivity were determined before and after oral glucose tolerance tests in 13 patients with CD of the terminal ileum, in 13 patients after resection of the terminal ileum and in 7 healthy controls. Basal and stimulated insulin sensitivities were determined using the homeostasis model assessment (HOMA) and the insulin sensitivity index (ISI) methods, respectively. Results: Basal and stimulated glucose levels were comparable in patients and controls. The peak stimulated GLP‐1 secretion was significantly higher in the patient group compared to controls: 12.2 ± 1.24 pM/L and 8.1 ± 1.72 pM/L, respectively, P = 0.03. This was associated with 52% increased overall insulin secretion in the patients' group as compared to controls (P = 0.007) and a higher peak insulin response: 63.5 ± 9.69 mU/L and 41.5 ± 6.85 mU/L for patients and controls, respectively, P = 0.04. Operated patients had similar GLP‐1 levels but higher peak and overall insulin secretions compared with those in non‐operated patients (P = 0.01). Fasting and stimulated insulin sensitivities were reduced only in patients with ileal resection as compared to controls: P = 0.01 and P = 0.05, respectively. No correlation was found between the CD activity index and GLP‐1 or insulin secretion. Conclusions: CD of the terminal ileum is associated with enhanced glucose‐dependent GLP‐1 secretion, which is unrelated to disease activity or ileal resection.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.