Evidence map›Paper›PMID 34777261›Full record

ReviewFrontiers in endocrinology2021

Endotoxins and Non-Alcoholic Fatty Liver Disease.

Takaomi Kessoku, Takashi Kobayashi, Kento Imajo, Kosuke Tanaka, Atsushi Yamamoto, Kota Takahashi, Yuki Kasai, Anna Ozaki, Michihiro Iwaki, Asako Nogami and 12 more

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
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

51 citing papers in PubMed.

  1. Review
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  10. [Role of Kupffer cells in liver regeneration with metabolic associated fatty liver disease in mice].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  11. Article
  12. Observational
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  14. Review
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  20. 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

22 authors.

Takaomi KessokuDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Takashi KobayashiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kento ImajoDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kosuke TanakaDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Atsushi YamamotoDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kota TakahashiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yuki KasaiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Anna OzakiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Michihiro IwakiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Asako NogamiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yasushi HondaDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yuji OgawaDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Shingo KatoDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Takuma HigurashiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kunihiro HosonoDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Masato YonedaDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Takayuki OkamotoDepartment of Pharmacology, Shimane University Faculty of Medicine, Izumo, Japan.
Haruki UsudaDepartment of Pharmacology, Shimane University Faculty of Medicine, Izumo, Japan.
Koichiro WadaDepartment of Pharmacology, Shimane University Faculty of Medicine, Izumo, Japan.
Noritoshi KobayashiDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Satoru SaitoDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Atsushi NakajimaDepartment of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. It occurs with a prevalence of up to 25%, of which 10-20% cases progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and liver cancer. The histopathology of NASH is characterized by neutrophilic infiltration, and endotoxins from gram-negative rods have been postulated as a contributing factor. Elevations in endotoxin levels in the blood can be classified as intestinal and hepatic factors. In recent years, leaky gut syndrome, which is characterized by impaired intestinal barrier function, has become a significant issue. A leaky gut may prompt intestinal bacteria dysbiosis and increase the amount of endotoxin that enters the liver from the portal vein. These contribute to persistent chronic inflammation and progressive liver damage. In addition, hepatic factors suggest that liver damage can be induced by low-dose endotoxins, which does not occur in healthy individuals. In particular, increased expression of CD14, an endotoxin co-receptor in the liver, may result in leptin-induced endotoxin hyper-responsiveness in obese individuals. Thus, elevated blood endotoxin levels contribute to the progression of NASH. The current therapeutic targets for NASH treat steatosis and liver inflammation and fibrosis. While many clinical trials are underway, no studies have been performed on therapeutic agents that target the intestinal barrier. Recently, a randomized placebo-controlled trial examined the role of the intestinal barrier in patients with NAFLD. To our knowledge, this study was the first of its kind and study suggested that the intestinal barrier may be a novel target in the future treatment of NAFLD.

Indexed as

Diet, High-FatEndotoxinsHumansLiverNon-alcoholic Fatty Liver DiseaseEndotoxinsendotoxinintestinal permeabilityleaky gutNAFLDsmall intestinal bacterial overgrowth

Identifiers

PMID34777261
PMCPMC8586459

What OpenQuestion holds

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Registered trials

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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.