Evidence map›Paper›PMID 29449623›Full record

ArticleInternational journal of obesity (2005)2018

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C.

S Becerril, A Rodríguez, V Catalán, L Méndez-Giménez, B Ramírez, N Sáinz, M Llorente, X Unamuno, J Gómez-Ambrosi, G Frühbeck

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Role of adipose tissue macrophages in obesity-related disorders.The Journal of experimental medicine · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Fight against fibrosis in adipose tissue remodeling.American journal of physiology. Endocrinology and metabolism · 2021
    Review
  13. Article
  14. Adipose tissue inflammation and metabolic dysfunction in obesity.American journal of physiology. Cell physiology · 2021
    Review
  15. Review
  16. Review
  17. Adipose Tissue Fibrosis: Mechanisms, Models, and Importance.International journal of molecular sciences · 2020
    Review
  18. Review
  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

10 authors at 3 institutions in 1 country.

S BecerrilMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
A RodríguezMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.ORCID http://orcid.org/0000-0002-2180-461X
V CatalánMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
L Méndez-GiménezMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
B RamírezMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
N SáinzMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
M LlorenteMedical Engineering Laboratory, University of Navarra, Pamplona, Spain.
X UnamunoMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
J Gómez-AmbrosiMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.ORCID http://orcid.org/0000-0001-5601-1604
G FrühbeckMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain. gfruhbeck@unav.es.
Instituto de Salud Carlos III · ESClinica Universidad de Navarra · ESUniversidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesObesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. SUBJECTS/

methodsThe expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg

resultsLeptin deficiency increased inflammation and fibrosis in AT. As expected, leptin treatment improved the obesity phenotype. iNOS deficiency in ob/ob mice improved insulin sensitivity, AT inflammation, and ECM remodeling, as evidenced by lower AT macrophage infiltration and collagen deposition, a downregulation of proinflammatory and profibrogenic genes Tnf, Emr1, Hif1a, Col6a1, Col6a3, and Tnc, as well as lower circulating TNC levels. Interestingly, leptin upregulated TNC expression and release in 3T3-L1 adipocytes, and iNOS knockdown in 3T3-L1 fat cells produced a significant decrease in basal and leptin-induced Tnc expression.

conclusionsAblation of iNOS in leptin-deficient mice improved AT inflammation and ECM remodeling-related genes, attenuating fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in adipocytes, suggesting an important role of this alarmin in the development of AT inflammation and fibrosis.

Indexed as

3T3-L1 CellsAdipose TissueAnimalsFibrosisGene SilencingInflammationLeptinMiceMice, KnockoutMice, ObeseNitric Oxide Synthase Type IIObesityTenascinLeptinNitric Oxide Synthase Type IINos2 protein, mouseTenascin

Identifiers

PMID29449623
OpenAlexW2792597790

What OpenQuestion holds

Textmetadata
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.