Abnormal post-prandial glucagon-like peptide release in patients with Crohn's disease

Background and aims: Glucagon-like peptide GLP-1 and -2 have been shown to regulate immune responses in immune-mediated disorders, including Crohn's disease (CD). Our aim was to investigate post-prandial GLP release and its potential link to chronic inflammation, insulin secretion/sensitivity and body composition changes in CD patients. Methods: Fifteen patients with CD, 15 healthy controls (HC) and 15 patients with metabolic syndrome (MS) were recruited. All patients underwent assessment of body composition by means of bio-impedance followed by a meal tolerance test (MTT). Only one CD patient did not tolerate the MTT and was excluded. Results: Basal GLP-1 levels were up-regulated in CD, however, as compared to HC, stimulated GLP-1 secretion was significantly reduced in CD (-31 %, p < 0.05) as in MS (-52 %, p < 0.003). Similarly, basal GLP-2 levels were comparable to that of HC, while response to MTT in CD was virtually absent (p < 0.05). Similar fasting insulin sensitivity, estimated 1stand 2nd phase insulin secretion and insulinogenic index were found in CD and in HC. Post-prandial GLP secretion waspositively correlated to insulin secretion indices, both in CD and MS. In CD, high-sensitive Creactive protein levels (hsCRP) and extra-cellular to intra-cellular water ratio (ECW/ICW), anindex of cellular inflammation, were inversely correlated with stimulated GLP-1 (p < 0.05 andp < 0.01, respectively) levels. Conclusion: CD is characterized by abnormal fasting and post-prandial GLP levels. Circulating GLP influences subclinical inflammation and glucose metabolism in CD patients, but not theirbody composition parameters. (C) 2020 Elsevier Masson SAS. All rights reserved.

Automated summary

CD patients show abnormal post-prandial GLP-1 and GLP-2 levels, which are correlated with chronic inflammation and insulin secretion/sensitivity, but not with body composition parameters.