Role of Bile Acids and GLP-1 in Mediating the Metabolic Improvements of Bariatric Surgery.
Anastomosis, Surgical
Animals
Anticholesteremic Agents
/ pharmacology
Bariatric Surgery
Bile Acids and Salts
/ metabolism
Blood Glucose
/ metabolism
Cholestyramine Resin
/ pharmacology
Diet, High-Fat
Gallbladder
/ surgery
Glucagon-Like Peptide 1
/ metabolism
Glucagon-Like Peptide-1 Receptor
/ antagonists & inhibitors
Glucose Tolerance Test
Ileum
/ surgery
Insulin Resistance
Intestines
/ microbiology
Lymph
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, Cytoplasmic and Nuclear
/ genetics
Receptors, G-Protein-Coupled
/ genetics
Signal Transduction
Verrucomicrobia
Weight Loss
Glucagon-Like Polypeptide 1 (Glp-1)
Gut Microbiome
Lymph Fistula
Metabolic Surgery
Journal
Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
02
08
2017
revised:
19
10
2018
accepted:
01
11
2018
pubmed:
18
11
2018
medline:
4
4
2019
entrez:
17
11
2018
Statut:
ppublish
Résumé
Bile diversion to the ileum (GB-IL) has strikingly similar metabolic and satiating effects to Roux-en-Y gastric bypass (RYGB) in rodent obesity models. The metabolic benefits of these procedures are thought to be mediated by increased bile acids, although parallel changes in body weight and other confounding variables limit this interpretation. Global G protein-coupled bile acid receptor-1 null (Tgr5 GB-IL induced weight loss and improved oral glucose tolerance in Tgr5 Bile diversion to the ileum improves glucose homeostasis via an intestinal Fxr-Glp-1 axis. Altered intestinal bile acid availability, independent of weight loss, and intestinal Akkermansia muciniphila appear to mediate the metabolic changes observed after bariatric surgery and might be manipulated for treatment of obesity and diabetes.
Sections du résumé
BACKGROUND & AIMS
Bile diversion to the ileum (GB-IL) has strikingly similar metabolic and satiating effects to Roux-en-Y gastric bypass (RYGB) in rodent obesity models. The metabolic benefits of these procedures are thought to be mediated by increased bile acids, although parallel changes in body weight and other confounding variables limit this interpretation.
METHODS
Global G protein-coupled bile acid receptor-1 null (Tgr5
RESULTS
GB-IL induced weight loss and improved oral glucose tolerance in Tgr5
CONCLUSIONS
Bile diversion to the ileum improves glucose homeostasis via an intestinal Fxr-Glp-1 axis. Altered intestinal bile acid availability, independent of weight loss, and intestinal Akkermansia muciniphila appear to mediate the metabolic changes observed after bariatric surgery and might be manipulated for treatment of obesity and diabetes.
Identifiants
pubmed: 30445014
pii: S0016-5085(18)35259-4
doi: 10.1053/j.gastro.2018.11.017
pmc: PMC6409186
mid: NIHMS1512400
pii:
doi:
Substances chimiques
Anticholesteremic Agents
0
Bile Acids and Salts
0
Blood Glucose
0
Glp1r protein, mouse
0
Glucagon-Like Peptide-1 Receptor
0
Gpbar1 protein, mouse
0
Receptors, Cytoplasmic and Nuclear
0
Receptors, G-Protein-Coupled
0
farnesoid X-activated receptor
0C5V0MRU6P
Cholestyramine Resin
11041-12-6
Glucagon-Like Peptide 1
89750-14-1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1041-1051.e4Subventions
Organisme : NIDDK NIH HHS
ID : U24 DK076169
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK105847
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NIDDK NIH HHS
ID : U2C DK059637
Pays : United States
Organisme : NIDDK NIH HHS
ID : F32 DK103474
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020593
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA068485
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK059637
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.
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