Evidence map›Paper›PMID 32390462›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2020

Lipopolysaccharides transport during fat absorption in rodent small intestine.

Yasutada Akiba, Koji Maruta, Takeshi Takajo, Kazuyuki Narimatsu, Hyder Said, Ikuo Kato, Atsukazu Kuwahara, Jonathan D Kaunitz

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 58 citations in OpenAlex.

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  6. Infection and immunity · 2026
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  20. Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Yasutada AkibaGreater Los Angeles Veterans Affairs Healthcare System, Los Angeles, California.ORCID 0000-0001-5731-1019
Koji MarutaDepartment of Medicine, University of California, School of Medicine, Los Angeles, California.
Takeshi TakajoDepartment of Medicine, University of California, School of Medicine, Los Angeles, California.
Kazuyuki NarimatsuDepartment of Medicine, University of California, School of Medicine, Los Angeles, California.
Hyder SaidDepartment of Medicine, University of California, School of Medicine, Los Angeles, California.
Ikuo KatoDepartment of Medical Biochemistry, Kobe Pharmaceutical University, Kobe, Japan.
Atsukazu KuwaharaResearch Unit for Epithelial Physiology, Research Organization of Science and Technology, Ritsumeikan University, Kusatsu, Japan.
Jonathan D KaunitzGreater Los Angeles Veterans Affairs Healthcare System, Los Angeles, California.ORCID 0000-0002-6064-5973
University of California, Los Angeles · USKobe Pharmaceutical University · JPRitsumeikan University · JP

Funding

Duodenal Muscosal Defense MechanismsR01DK054221 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KAUNITZ, JONATHAN D. · 1999 to 2016
$4.4M
BLRD VA I01 BX001245NIDDK NIH HHS R01 DK054221
6 · The paper itself

Abstract

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

Indexed as

AnimalsBiological TransportFatsGastrointestinal AgentsHEK293 CellsHumansIntestine, SmallLipopolysaccharidesMaleMiceMice, Inbred C57BLPeptidesRatsRats, Sprague-DawleyToll-Like Receptor 4FatsGastrointestinal AgentsLipopolysaccharidesPeptidesteduglutideToll-Like Receptor 4CD36GLP-2LCFA absorptionlipid raftLPS transport

Identifiers

PMID32390462
PMCPMC7311662
OpenAlexW3021126227

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.