Evidence map›Paper›PMID 39408569›Full record

ArticleInternational journal of molecular sciences2024

Evidence for a Pro-Inflammatory State of Macrophages from Non-Obese Type-2 Diabetic Goto-Kakizaki Rats.

Amanda Santos de Almeida Silveira, Amara Cassandra Dos Anjos Alves, Gabriela Mandú Gimenes, Patrícia da Silva Quessada, Tiago Bertola Lobato, Beatriz Belmiro Dias, Ana Carolina Gomes Pereira, Patrícia Nancy Iser-Bem, Joice Naiara Bertaglia Pereira, Elaine Hatanaka and 7 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

17 authors.

Amanda Santos de Almeida SilveiraInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0003-1041-7646
Amara Cassandra Dos Anjos AlvesInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.
Gabriela Mandú GimenesInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-3432-1668
Patrícia da Silva QuessadaInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.
Tiago Bertola LobatoInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0003-1100-4050
Beatriz Belmiro DiasInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-8407-0975
Ana Carolina Gomes PereiraInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.
Patrícia Nancy Iser-BemInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-0053-3777
Joice Naiara Bertaglia PereiraInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0003-2609-5450
Elaine HatanakaInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-9716-1163
Laureane Nunes MasiMulticenter Graduate Program in Physiological Sciences, Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis, SC 88037-000, Brazil.ORCID 0000-0001-9472-7304
Tânia Cristina Pithon-CuriInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.
Vânia Gomes de Moura MattaraiaButantan Institute, São Paulo 05585-000, SP, Brazil.ORCID 0000-0001-9099-3963
Sandro Massao HirabaraInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-7392-0444
Amanda Rabello CrismaDepartment of Clinical Analysis, Federal University of Paraná, Curitiba 80210-170, PR, Brazil.
Renata GorjãoInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.ORCID 0000-0002-9655-1477
Rui CuriInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo 01506-000, SP, Brazil.

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/09868-7
6 · The paper itself

Abstract

Obesity causes insulin resistance (IR) through systemic low-grade inflammation and can lead to type 2 diabetes mellitus (T2DM). However, the mechanisms that cause IR and T2DM in non-obese individuals are unclear. The Goto-Kakizaki (GK) rat develops IR spontaneously and is a model of non-obese T2DM. These rats exhibit hyperglycemia beginning at weaning and exhibit lower body mass than control Wistar rats. Herein, we tested the hypothesis that macrophages of GK rats are permanently in a pro-inflammatory state, which may be associated with a systemic inflammation condition that mimics the pathogenesis of obesity-induced T2DM. Using eighteen-week-old GK and control Wistar rats, we investigated the proportions of M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophages isolated from the peritoneal cavity. Additionally, the production of inflammatory cytokines and reactive oxygen species (ROS) in cultured macrophages under basal and stimulated conditions was assessed. It was found that phorbol myristate acetate (PMA) stimulation increased GK rat macrophage ROS production 90-fold compared to basal levels. This response was also three times more pronounced than in control cells (36-fold). The production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), tended to be upregulated in cultured macrophages from GK rats under basal conditions. Macrophages from GK rats produced 1.6 times more granulocyte-macrophage colony-stimulating factor (GM-CSF), 1.5 times more monocyte chemoattractant protein-1 (MCP-1) and 3.3 times more TNF-α than control cells when stimulated with lipopolysaccharide (LPS) (

Indexed as

Diabetes Mellitus, Type 2InflammationMacrophagesRats, WistarReactive Oxygen SpeciesAnimalsCytokinesDisease Models, AnimalInsulin ResistanceMaleRatsTumor Necrosis Factor-alphaCytokinesReactive Oxygen SpeciesTumor Necrosis Factor-alphaGKGM-CSFinflammationinsulin resistanceM1M2TNF-αtype 2 diabetes mellitus

Identifiers

PMID39408569
PMCPMC11477416

What Socratic 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 Socratic graph.