Evidence map›Paper›PMID 24858832›Full record

ArticlePloS one2014

β-Cryptoxanthin alleviates diet-induced nonalcoholic steatohepatitis by suppressing inflammatory gene expression in mice.

Masuko Kobori, Yinhua Ni, Yumiko Takahashi, Natsumi Watanabe, Minoru Sugiura, Kazunori Ogawa, Mayumi Nagashimada, Shuichi Kaneko, Shigehiro Naito, Tsuguhito Ota

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
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  6. Targeting hepatic macrophages for non-alcoholic fatty liver disease therapy.Frontiers in cell and developmental biology · 2024
    Review
  7. Review
  8. β-cryptoxanthin and fatty liver disease: new insights.Hepatobiliary surgery and nutrition · 2023
    Article
  9. Article
  10. Review
  11. Article
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  14. Article
  15. Article
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  17. Pirfenidone prevents and reverses hepatic insulin resistance and steatohepatitis by polarizing M2 macrophages.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  18. 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

10 authors at 4 institutions in 1 country.

Masuko KoboriNational Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Yinhua NiDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa, Japan; Department of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan.
Yumiko TakahashiNational Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Natsumi WatanabeNational Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Minoru SugiuraCitrus Research Division, NARO Institute of Fruit Tree Science, National Agriculture and Food Research Organization, Shimizu, Shizuoka, Japan.
Kazunori OgawaGrape and Persimmon Research Division, NARO Institute of Fruit Tree Science, National Agriculture and Food Research Organization, Higashi-hiroshima, Hiroshima, Japan.
Mayumi NagashimadaDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa, Japan.
Shuichi KanekoDepartment of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan.
Shigehiro NaitoNational Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Tsuguhito OtaDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa, Japan; Department of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan.
Kanazawa University · JPNational Agriculture and Food Research Organization · JPFood Research Institute · JPShimizu (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent nutritional epidemiological surveys showed that serum β-cryptoxanthin inversely associates with the risks for insulin resistance and liver dysfunction. Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance and oxidative stress from nonalcoholic fatty liver disease. To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes in NASH. Increased levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) were reduced by β-cryptoxanthin in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH.

Indexed as

AnimalsAntigens, DifferentiationCholesterolCryptoxanthinsDietary FatsGene Expression RegulationInflammationInsulin ResistanceMacrophagesMaleMiceNon-alcoholic Fatty Liver DiseaseT-LymphocytesAntigens, DifferentiationCholesterolCryptoxanthinsDietary Fats

Identifiers

PMID24858832
PMCPMC4032271
OpenAlexW2077569421

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.