MON-589 studying mechanisms of satiety in the human ileum and colon
File(s)
Published version
Author(s)
Type
Journal Article
Abstract
Background The gut-brain axis plays important roles in the regulation of appetite and glucose homeostasis. The presence of nutrients and their digestive products in specific regions of the gastrointestinal tract modulates neuronal and hormonal signalling, including the release of the appetite-suppressing gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). While there has been significant research into the upper gut mechanisms behind satiation, i.e. the termination of meal, the role of the ileum and colon in satiety, i.e. the process which delays a subsequent meal, has been relatively little investigated, particularly in humans. Methods Ten healthy volunteers attended our Clinical Research Facility for two visits of four days each. At each visit they had either a nasoileal or a nasocolonic tube inserted under fluoroscopy. They were then provided a diet rich in protein and fibre to promote satiety. Gut contents and blood samples were taken before and during test meals at the start and end of the visit, and visual analogue scales were used to measure subjective feelings of appetite. Metabonomic analysis of gut fluid was carried out using a combination of in-house NMR and LC-MS-based methods. 16S rRNA gene sequencing was used to investigate effects on the colonic microbiome. Circulating levels of glucose, the gut hormones GLP-1 and PYY, and the pancreatic hormones insulin and glucagon were measured. Results and discussion The test meals resulted in sustained suppression of appetite and release of GLP-1 and PYY. Ileal and colonic microbial profiles were distinct from those identified in stool samples, and changed with adaptation to the high protein and fibre diet. Integrating hormonal, metabonomic and bacterial datasets from these human studies gives insight into how nutrient and metabolite sensing in the gastrointestinal tract regulates appetite and glucose homeostasis, and may suggest novel therapeutic targets for metabolic disease.
Date Issued
2020-05-08
Date Acceptance
2020-05-01
Citation
Journal of the Endocrine Society, 2020, 4 (Supplement_1), pp.A750-A750
ISSN
2472-1972
Publisher
Oxford University Press
Start Page
A750
End Page
A750
Journal / Book Title
Journal of the Endocrine Society
Volume
4
Issue
Supplement_1
Copyright Statement
© Endocrine Society 2020.
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
Identifier
https://academic.oup.com/jes/article/4/Supplement_1/MON-589/5833351
Publication Status
Published
Date Publish Online
2020-05-08