Abnormal post-prandial glucagon-like peptide release in patients with Crohn's disease - 07/10/20

Doi : 10.1016/j.clinre.2020.08.011

Pietro Lucotti ^a, Elisabetta Lovati ^a, Marco Vincenzo Lenti ^a, Beatrice Valvo ^a, Elisa Sprio ^a, Nicola Aronico ^a, Paolo Giuffrida ^a, Dominica Dell’Aera ^a, Alessandra Pasini ^a, Cristina Ubezio ^a, Mariangela Delliponti ^a, Carmine Tinelli ^b, Gino Roberto Corazza ^a, Antonio Di Sabatino ^a,⁎
^a First Department of Internal Medicine, San Matteo Hospital Foundation, University of Pavia, Pavia, Italy
^b Clinical Epidemiology and Biometric Unit, San Matteo Hospital Foundation, Pavia, Italy

^⁎Corresponding author at: Clinica Medica, Fondazione IRCCS Policlinico San Matteo, Università di Pavia, Piazzale Golgi 19, 27100 Pavia, Italy.Clinica MedicaFondazione IRCCS Policlinico San MatteoUniversità di PaviaPiazzale Golgi 19Pavia27100Italy

Sous presse. Épreuves corrigées par l'auteur. Disponible en ligne depuis le Wednesday 07 October 2020
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Highlights

•	What is already known on this subject?
•	Glucagon-like peptide (GLP)-1 and -2 have been shown to regulate immune responses in immune-mediated disorders, such as Crohn’s disease (CD)
•	What are the new findings?
•	Basal GLP-1 levels were up-regulated in CD, while GLP-1 secretion was significantly reduced compared to healthy volunteers (HV) and patients with metabolic syndrome (MS)
•	Post-prandial GLP secretion was positively correlated to insulin secretion indices, both in CD and MS
•	How might it impact on clinical practice in the foreseeable future?
•	Future research should focus on metabolic alterations and GLP secretion in patients with CD, as these may represent therapeutic targets

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Abstract

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 1^st and 2^nd phase insulin secretion and insulinogenic index were found in CD and in HC. Post-prandial GLP secretion was positively correlated to insulin secretion indices, both in CD and MS. In CD, high-sensitive C reactive protein levels (hsCRP) and extra-cellular to intra-cellular water ratio (ECW/ICW), an index of cellular inflammation, were inversely correlated with stimulated GLP-1 (p < 0.05 and p < 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 their body composition parameters.

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Abbreviations : BIA, CD, ECW:ICW, EEC, FFM, FFMI, FM, GLP, HC, hsCRP, IBD, i-FABP, IGI, IMAT, MS, MTT