Gastrointestinal peptides and small-bowel hypomotility are possible causes for fasting and postprandial symptoms in active Crohn's disease.


Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
01 01 2020
Historique:
received: 24 02 2019
accepted: 29 08 2019
pubmed: 27 9 2019
medline: 28 4 2020
entrez: 27 9 2019
Statut: ppublish

Résumé

Crohn's disease (CD) patients suffer postprandial aversive symptoms, which can lead to anorexia and malnutrition. Changes in the regulation of gut hormones and gut dysmotility are believed to play a role. This study aimed to investigate small-bowel motility and gut peptide responses to a standard test meal in CD by using MRI. We studied 15 CD patients with active disease (age 36 ± 3 y; BMI 26 ± 1 kg/m 2) and 20 healthy volunteers (HVs; age 31 ± 3 years; BMI 24 ± 1 kg/m 2). They underwent baseline and postprandial MRI scans, symptom questionnaires, and blood sampling following a 400-g soup meal (204 kcal). Small-bowel motility, other MRI parameters, and glucagon-like peptide-1 (GLP-1), polypeptide YY (PYY), and cholecystokinin peptides were measured. Data are presented as means ± SEMs. HVs had significantly higher fasting motility indexes [106 ± 13 arbitrary units (a.u.)], compared with CD participants (70 ± 8 a.u.; P ≤ 0.05). Postprandial small-bowel water content showed a significant time by group interaction (P < 0.05), with CD participants showing higher levels from 210 min postprandially. Fasting concentrations of GLP-1 and PYY were significantly greater in CD participants, compared with HVs [GLP-1, CD 50 ± 8 µg/mL versus HV 13 ± 3 µg/mL (P ≤ 0.0001); PYY, CD 236 ± 16 pg/mL versus HV 118 ± 12 pg/mL (P ≤ 0.0001)]. The meal challenge induced a significant postprandial increase in aversive symptom scores (fullness, distention, bloating, abdominal pain, and sickness) in CD participants compared with HVs (P ≤ 0.05). The decrease in fasting small-bowel motility noted in CD participants can be ascribed to the increased fasting gut peptides. A better understanding of the etiology of aversive symptoms in CD will facilitate identification of better therapeutic targets to improve nutritional status. This trial was registered at clinicaltrials.gov as NCT03052465.

Sections du résumé

BACKGROUND
Crohn's disease (CD) patients suffer postprandial aversive symptoms, which can lead to anorexia and malnutrition. Changes in the regulation of gut hormones and gut dysmotility are believed to play a role.
OBJECTIVES
This study aimed to investigate small-bowel motility and gut peptide responses to a standard test meal in CD by using MRI.
METHODS
We studied 15 CD patients with active disease (age 36 ± 3 y; BMI 26 ± 1 kg/m 2) and 20 healthy volunteers (HVs; age 31 ± 3 years; BMI 24 ± 1 kg/m 2). They underwent baseline and postprandial MRI scans, symptom questionnaires, and blood sampling following a 400-g soup meal (204 kcal). Small-bowel motility, other MRI parameters, and glucagon-like peptide-1 (GLP-1), polypeptide YY (PYY), and cholecystokinin peptides were measured. Data are presented as means ± SEMs.
RESULTS
HVs had significantly higher fasting motility indexes [106 ± 13 arbitrary units (a.u.)], compared with CD participants (70 ± 8 a.u.; P ≤ 0.05). Postprandial small-bowel water content showed a significant time by group interaction (P < 0.05), with CD participants showing higher levels from 210 min postprandially. Fasting concentrations of GLP-1 and PYY were significantly greater in CD participants, compared with HVs [GLP-1, CD 50 ± 8 µg/mL versus HV 13 ± 3 µg/mL (P ≤ 0.0001); PYY, CD 236 ± 16 pg/mL versus HV 118 ± 12 pg/mL (P ≤ 0.0001)]. The meal challenge induced a significant postprandial increase in aversive symptom scores (fullness, distention, bloating, abdominal pain, and sickness) in CD participants compared with HVs (P ≤ 0.05).
CONCLUSIONS
The decrease in fasting small-bowel motility noted in CD participants can be ascribed to the increased fasting gut peptides. A better understanding of the etiology of aversive symptoms in CD will facilitate identification of better therapeutic targets to improve nutritional status. This trial was registered at clinicaltrials.gov as NCT03052465.

Identifiants

pubmed: 31557279
pii: S0002-9165(22)00980-7
doi: 10.1093/ajcn/nqz240
doi:

Substances chimiques

Gastrointestinal Hormones 0
Peptide YY 106388-42-5
Glucagon-Like Peptide 1 89750-14-1
Cholecystokinin 9011-97-6

Banques de données

ClinicalTrials.gov
['NCT03052465']

Types de publication

Clinical Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

131-140

Subventions

Organisme : Department of Health
ID : EME/14/201/16
Pays : United Kingdom

Informations de copyright

Copyright © American Society for Nutrition 2019. All rights reserved.

Auteurs

Asseel Khalaf (A)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Caroline L Hoad (CL)

National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.
Sir Peter Mansfield Imaging Centre, School of Physics and Astronomy, University of Nottingham, Nottingham, United Kingdom.

Alex Menys (A)

Motilent Ltd, London, United Kingdom.

Adam Nowak (A)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Shellie Radford (S)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Stuart A Taylor (SA)

Centre for Medical Imaging, Division of Medicine, University College London, United Kingdom.

Khalid Latief (K)

Department of Radiology, Nottingham University Hospitals, Nottingham, United Kingdom.

Melanie Lingaya (M)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Yirga Falcone (Y)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Gulzar Singh (G)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Robin C Spiller (RC)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Penny A Gowland (PA)

National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.
Sir Peter Mansfield Imaging Centre, School of Physics and Astronomy, University of Nottingham, Nottingham, United Kingdom.

Luca Marciani (L)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

Gordon W Moran (GW)

Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
National Institute of Health Research Nottingham Biomedical Research Centre at Nottingham University, Hospitals National Health Service Trust and the University of Nottingham, Nottingham, United Kingdom.

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