Evidence map›Paper›PMID 32235497›Full record

ArticleNutrients2020

Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis.

Anja Baumann, Cheng Jun Jin, Annette Brandt, Cathrin Sellmann, Anika Nier, Markus Burkard, Sascha Venturelli, Ina Bergheim

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 4 pooled it
4.1field-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

30 citing papers in PubMed, 4 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Article
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  15. Gut microbiome in non-alcoholic fatty liver disease.Frontiers in gastroenterology (Lausanne, Switzerland) · 2024
    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

8 authors at 3 institutions in 2 countries.

Anja BaumannDepartment of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria.
Cheng Jun JinInstitute of Nutritional Sciences, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Straße 22-25, 07743 Jena, Germany.
Annette BrandtDepartment of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria.
Cathrin SellmannInstitute of Nutritional Sciences, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Straße 22-25, 07743 Jena, Germany.
Anika NierDepartment of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria.
Markus BurkardInstitute of Physiology, Department of Vegetative and Clinical Physiology, University Hospital Tuebingen, Wilhelmstraße 56, 72074 Tuebingen, Germany.
Sascha VenturelliInstitute of Physiology, Department of Vegetative and Clinical Physiology, University Hospital Tuebingen, Wilhelmstraße 56, 72074 Tuebingen, Germany.
Ina BergheimDepartment of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria.
University of Vienna · ATFriedrich Schiller University Jena · DEUniversity of Hohenheim · DE

Funding

Bundesministerium für Bildung und Forschung FKZ: 01EA1305 to I.B.
6 · The paper itself

Abstract

Sodium butyrate (SoB) supplementation has been suggested to attenuate the development of non-alcoholic fatty liver disease (NAFLD). Here, we determined the therapeutic potential of SoB on NAFLD progression and molecular mechanism involved. Eight-week old C57BL/6J mice were pair-fed a fat-, fructose- and cholesterol-rich diet (FFC) or control diet (C). After 8 weeks, some mice received 0.6g SoB/kg bw in their respective diets (C+SoB; FFC+SoB) or were maintained on C or FFC for the next 5 weeks of feeding. Liver damage, markers of glucose metabolism, inflammation, intestinal barrier function and melatonin metabolism were determined. FFC-fed mice progressed from simple steatosis to early non-alcoholic steatohepatitis, along with significantly higher TNFα and IL-6 protein levels in the liver and impaired glucose tolerance. In FFC+SoB-fed mice, disease was limited to steatosis associated with protection against the induction of

Indexed as

Dietary SupplementsAnimalsButyric AcidCholesterol, DietaryDiet, High-FatDisease Models, AnimalDisease ProgressionFemaleGlucoseInflammationInterleukin-6Intestine, SmallLiverMelatoninMice, Inbred C57BLNitric Oxide Synthase Type IIButyric AcidCholesterol, DietaryGlucoseInterleukin-6MelatoninNitric Oxide Synthase Type IINos2 protein, mouseTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alphainducible nitric oxide synthasemelatonin synthesisnon-alcoholic steatohepatitissodium butyratetoll-like receptor 4

Identifiers

PMID32235497
PMCPMC7231312
OpenAlexW3013928862

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.