Evidence map›Paper›PMID 20596733›Full record

ArticleJournal of gastroenterology2010

Absence of invariant natural killer T cells deteriorates liver inflammation and fibrosis in mice fed high-fat diet.

Takuya Miyagi, Tetsuo Takehara, Akio Uemura, Kumiko Nishio, Satoshi Shimizu, Takahiro Kodama, Hayato Hikita, Wei Li, Akira Sasakawa, Tomohide Tatsumi and 4 more

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  7. Effects of NKT Cells on Metabolic Disorders Caused by High-Fat Diet Using CD1d-Knockout Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
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  15. The Roles of Immune Cells in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2020
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  17. Review
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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

14 authors at 1 institution in 1 country.

Takuya MiyagiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Tetsuo Takehara
Akio Uemura
Kumiko Nishio
Satoshi Shimizu
Takahiro Kodama
Hayato Hikita
Wei Li
Akira Sasakawa
Tomohide Tatsumi
Kazuyoshi Ohkawa
Tatsuya Kanto
Naoki Hiramatsu
Norio Hayashi
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInvariant natural killer T (iNKT) cells have been suggested to play critical roles in a wide range of immune responses by acting in a proinflammatory or anti-inflammatory manner. Nonalcoholic steatohepatitis (NASH) is a chronic liver disease progressing to advanced cirrhosis and hepatocellular carcinoma. Despite the abundance of iNKT cells in the liver, their role in the pathogenesis of NASH remains obscure. Here, we investigated their role in the development of diet-induced steatosis/steatohepatitis.

methodsWe used BALB/c wild-type mice and Jα18-deficient (KO) mice lacking iNKT cells fed either a normal diet or a high-fat diet (HFD). The liver and blood were collected from these mice to examine liver inflammation, steatosis, and fibrosis at the indicated time points.

resultsKO mice fed the HFD, compared with control mice fed the HFD, exhibited a clearly higher serum alanine aminotransferase level and a greater number of hepatic inflammatory foci, although there was no significant difference in hepatic lipid retention between these groups of mice. The HFD enhanced hepatic messenger RNA expression of inflammatory cytokines and chemokines in KO but not in control mice. The HFD also increased the proportion of hepatic CD4 T cells and CD8 T cells that composed hepatic inflammatory foci in KO mice, but not in the controls. Prolonged feeding with the HFD augmented liver fibrosis in KO but not in control mice.

conclusionsThese findings indicate that iNKT cells play a protective role against liver inflammation progressing to fibrosis, but not against steatosis, enhanced by dietary excess fat, suggesting a key role of these cells in NASH pathogenesis.

Indexed as

AnimalsDietary FatsDisease Models, AnimalFatty LiverInflammationLiverLiver CirrhosisMaleMiceMice, Inbred BALB CMice, KnockoutNatural Killer T-CellsReceptors, Antigen, T-Cell, alpha-betaTime FactorsDietary FatsReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID20596733
OpenAlexW2000836997

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.