Evidence map›Paper›PMID 31349725›Full record

ArticleCells2019

Immune-Deficient Pfp/Rag2

Sandra Winkler, Madlen Hempel, Mei-Ju Hsu, Martin Gericke, Hagen Kühne, Sandra Brückner, Silvio Erler, Ralph Burkhardt, Bruno Christ

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Molecular genetics and metabolism reports · 2020
    Article
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 2 institutions in 1 country.

Sandra WinklerDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany.
Madlen HempelDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany.
Mei-Ju HsuDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany.
Martin GerickeInstitute of Anatomy and Cell Biology, Martin-Luther University Halle-Wittenberg, 06108 Halle (Saale), Germany.
Hagen KühneDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany.
Sandra BrücknerDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany.
Silvio ErlerInstitute of Biology, Animal Ecology, Martin-Luther-University Halle-Wittenberg, 06099 Halle, Germany.
Ralph BurkhardtInstitute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig, 04103 Leipzig, Germany.
Bruno ChristDepartment of Visceral-, Transplantation, Thoracic and Vascular Surgery, Division of Applied Molecular Hepatology, University of Leipzig, 04103 Leipzig, Germany. bruno.christ@medizin.uni-leipzig.de.
Leipzig University · DEMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a risk factor for adipose tissue dysfunction, which is associated with inflammatory innate immune mechanisms. Since the adipose tissue/liver axis contributes to hepatosteatosis, we sought to determine age-related adipose tissue dysfunction in the context of the activation of the innate immune system fostering fatty liver phenotypes. Using wildtype and immune-deficient mice, we compared visceral adipose tissue and liver mass as well as hepatic lipid storage in young (ca. 14 weeks) and adult (ca. 30 weeks) mice. Adipocyte size was determined as an indicator of adipocyte function and liver steatosis was quantified by hepatic lipid content. Further, lipid storage was investigated under normal and steatosis-inducing culture conditions in isolated hepatocytes. The physiological age-related increase in body weight was associated with a disproportionate increase in adipose tissue mass in immune-deficient mice, which coincided with higher triglyceride storage in the liver. Lipid storage was similar in isolated hepatocytes from wildtype and immune-deficient mice under normal culture conditions but was significantly higher in immune-deficient than in wildtype hepatocytes under steatosis-inducing culture conditions. Immune-deficient mice also displayed increased inflammatory, adipogenic, and lipogenic markers in serum and adipose tissue. Thus, the age-related increase in body weight coincided with an increase in adipose tissue mass and hepatic steatosis. In association with a (pro-)inflammatory milieu, aging thus promotes hepatosteatosis, especially in immune-deficient mice.

Indexed as

AdipocytesAdipose TissueAnimalsDNA-Binding ProteinsFatty LiverFemaleGene Expression ProfilingHepatocytesImmunologic Deficiency SyndromesLipid MetabolismLiverMaleMiceMice, Inbred C57BLMice, KnockoutPhenotypeDNA-Binding ProteinsRag2 protein, mouseadipose tissueaginghepatocytehepatosteatosisinnate immune systemliver

Identifiers

PMID31349725
PMCPMC6721582
OpenAlexW2963187475

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.