Evidence map›Paper›PMID 33050035›Full record

ArticleCells2020

Kupffer Cells Sense Free Fatty Acids and Regulate Hepatic Lipid Metabolism in High-Fat Diet and Inflammation.

Kira L Diehl, Julia Vorac, Kristina Hofmann, Philippa Meiser, Iris Unterweger, Lars Kuerschner, Heike Weighardt, Irmgard Förster, Christoph Thiele

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
  2. Article
  3. Kupffer cells: Orchestrators of liver physiology.Liver research (Beijing, China) · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

9 authors at 1 institution in 1 country.

Kira L DiehlLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Julia VoracLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Kristina HofmannLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Philippa MeiserLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Iris UnterwegerLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Lars KuerschnerLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.ORCID 0000-0003-4783-0442
Heike WeighardtLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.
Irmgard FörsterLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.ORCID 0000-0002-7644-5642
Christoph ThieleLife and Medical Science Institute (LIMES), University of Bonn, Carl-Troll-Straße 31, 53115 Bonn, Germany.ORCID 0000-0001-5161-2558
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A high fat Western-style diet leads to hepatic steatosis that can progress to steatohepatitis and ultimately cirrhosis or liver cancer. The mechanism that leads to the development of steatosis upon nutritional overload is complex and only partially understood. Using click chemistry-based metabolic tracing and microscopy, we study the interaction between Kupffer cells and hepatocytes ex vivo. In the early phase of steatosis, hepatocytes alone do not display significant deviations in fatty acid metabolism. However, in co-cultures or supernatant transfer experiments, we show that tumor necrosis factor (TNF) secretion by Kupffer cells is necessary and sufficient to induce steatosis in hepatocytes, independent of the challenge of hepatocytes with elevated fatty acid levels. We further show that free fatty acid (FFA) or lipopolysaccharide are both able to trigger release of TNF from Kupffer cells. We conclude that Kupffer cells act as the primary sensor for both FFA overload and bacterial lipopolysaccharide, integrate these signals and transmit the information to the hepatocyte via TNF secretion. Hepatocytes react by alteration in lipid metabolism prominently leading to the accumulation of triacylglycerols (TAGs) in lipid droplets, a hallmark of steatosis.

Indexed as

AnimalsClick ChemistryDiet, High-FatDisease Models, AnimalFatty Acids, NonesterifiedFatty LiverHepatocytesInflammationKupffer CellsLipid MetabolismLipidsLiverMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseFatty Acids, NonesterifiedLipidsTumor Necrosis Factor-alphalipids/chemistrymetabolic diseasenon-alcoholic fatty liver diseasenutrition/lipids

Identifiers

PMID33050035
PMCPMC7600268
OpenAlexW3092407918

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.