Lipopolysaccharides transport during fat absorption in rodent small intestine.
CD36
GLP-2
LCFA absorption
LPS transport
lipid raft
Journal
American journal of physiology. Gastrointestinal and liver physiology
ISSN: 1522-1547
Titre abrégé: Am J Physiol Gastrointest Liver Physiol
Pays: United States
ID NLM: 100901227
Informations de publication
Date de publication:
01 06 2020
01 06 2020
Historique:
pubmed:
12
5
2020
medline:
21
10
2020
entrez:
12
5
2020
Statut:
ppublish
Résumé
Lipopolysaccharides (LPS) are potent pro-inflammatory molecules that enter the systemic circulation from the intestinal lumen by uncertain mechanisms. We investigated these mechanisms and the effect of exogenous glucagon-like peptide-2 (GLP-2) on LPS transport in the rodent small intestine. Transmucosal LPS transport was measured in Ussing-chambered rat jejunal mucosa. In anesthetized rats, the appearance of fluorescein isothiocyanate (FITC)-LPS into the portal vein (PV) and the mesenteric lymph was simultaneously monitored after intraduodenal perfusion of FITC-LPS with oleic acid and taurocholate (OA/TCA). In vitro, luminally applied LPS rapidly appeared in the serosal solution only with luminal OA/TCA present, inhibited by the lipid raft inhibitor methyl-β-cyclodextrin (MβCD) and the CD36 inhibitor sulfosuccinimidyl oleate (SSO), or by serosal GLP-2. In vivo, perfusion of FITC-LPS with OA/TCA rapidly increased FITC-LPS appearance into the PV, followed by a gradual increase of FITC-LPS into the lymph. Rapid PV transport was inhibited by the addition of MβCD or by SSO, whereas transport into the lymph was inhibited by chylomicron synthesis inhibition. Intraveous injection of the stable GLP-2 analog teduglutide acutely inhibited FITC-LPS transport into the PV, yet accelerated FITC-LPS transport into the lymph via
Identifiants
pubmed: 32390462
doi: 10.1152/ajpgi.00079.2020
pmc: PMC7311662
doi:
Substances chimiques
Fats
0
Gastrointestinal Agents
0
Lipopolysaccharides
0
Peptides
0
Toll-Like Receptor 4
0
teduglutide
7M19191IKG
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
G1070-G1087Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK054221
Pays : United States
Organisme : HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
ID : R01 DK54221
Pays : International
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