Evidence map›Paper›PMID 39004641›Full record

ArticleInternational journal of obesity (2005)2024

Characterization of obesity-related diseases and inflammation using single cell immunophenotyping in two different diet-induced obesity models.

Zsófia Ruppert, Patrícia Neuperger, Bettina Rákóczi, Nikolett Gémes, Brigitta Dukay, Petra Hajdu, Mária Péter, Gábor Balogh, László Tiszlavicz, László Vígh and 4 more

Abstract read
In one paragraph

Article in International journal of obesity (2005), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
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  9. Review
  10. Article
  11. Sex-Dependent T Cell Dysregulation in Mice with Diet-Induced Obesity.International journal of molecular sciences · 2024
    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

14 authors.

Zsófia Ruppert *Laboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Patrícia Neuperger *PhD School in Biology, University of Szeged, Szeged, Hungary.
Bettina RákócziLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Nikolett GémesPhD School in Biology, University of Szeged, Szeged, Hungary.
Brigitta DukayLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Petra HajduLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Mária PéterLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Gábor BaloghLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
László TiszlaviczDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
László VíghLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
Zsolt TörökLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary.
László G PuskásLaboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Centre, Szeged, Hungary.
Gábor J SzebeniLaboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Centre, Szeged, Hungary. szebeni.gabor@brc.hu.
Melinda E TóthLaboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary. toth.erzsebetmelinda@brc.hu.ORCID 0000-0002-5529-6967

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is a growing problem worldwide and a major risk factor for many chronic diseases. The accumulation of adipose tissue leads to the release of significant amounts of pro-inflammatory cytokines and adipokines, resulting in a low-grade systemic inflammation. However, the mechanisms behind the development of obesity-related diseases are not fully understood. Therefore, our study aimed to investigate the pathological changes and inflammatory processes at systemic level and in individual organs in two different diet-induced mouse obesity models.

methodsMale C57BL6/J mice were fed by high-fat diet (HFD), high-fat/high-fructose diet (HFD + FR) or normal chow for 21 weeks starting at 3 months of age (n = 15 animals/group). Insulin resistance was tested by oral glucose tolerance test. Pathological changes were investigated on hematoxylin-eosin-stained liver and brown adipose tissue sections. The gene expression levels of adipokines and cytokines were analyzed by qPCR in adipose tissues, whereas serum protein concentrations were determined by multiplex immunoassays. Immunophenotyping of isolated blood, bone marrow and spleen cells was performed by single-cell mass cytometry.

resultsWeight gain, glucose intolerance and hepatic steatosis were more severe in the HFD + FR group than in the control and HFD groups. This was accompanied by a higher level of systemic inflammation, as indicated by increased expression of pro-inflammatory genes in visceral white adipose tissue and by a higher serum TNFα level. In addition, immunophenotyping revealed the increase of the surface expressions of CD44 and CD69 on various cell types, such as CD8+ and CD4 + T-cells, B-cells and macrophages, in animals with obesity.

conclusionsThe combination of HFD with fructose supplementation promotes more properly the symptoms of metabolic syndrome. Therefore, the combined high-fat/high-fructose nutrition can be a more suitable model of the Western diet. However, despite these differences, both models showed immunophenotypic changes that may be associated with increased risk of obesity-related cancer.

Indexed as

Diet, High-FatDisease Models, AnimalImmunophenotypingInflammationMice, Inbred C57BLObesityAdipokinesAdipose TissueAnimalsInsulin ResistanceMaleMiceAdipokines

Identifiers

PMID39004641
PMCPMC11502477

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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.