Evidence map›Paper›PMID 27057272›Full record

ArticleOxidative medicine and cellular longevity2016

Aging Increases Susceptibility to High Fat Diet-Induced Metabolic Syndrome in C57BL/6 Mice: Improvement in Glycemic and Lipid Profile after Antioxidant Therapy.

Valéria Nunes-Souza, Cheila Juliana César-Gomes, Lucas José Sá Da Fonseca, Glaucevane Da Silva Guedes, Salete Smaniotto, Luíza Antas Rabelo

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

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  19. The role of aging in cancer.Molecular oncology · 2022
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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

6 authors at 4 institutions in 3 countries.

Valéria Nunes-SouzaLaboratório de Reatividade Cardiovascular (LRC), Núcleo de Síndrome Metabólica, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil; National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Avenida Antônio Carlos, s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil; Departamento de Fisiologia e Farmacologia, Centro de Ciências Biológicas (CCB), Universidade Federal de Pernambuco (UFPE), Avenida Professor Moraes Rego 1235, Cidade Universitária, 50670-901 Recife, PE, Brazil.
Cheila Juliana César-GomesLaboratório de Reatividade Cardiovascular (LRC), Núcleo de Síndrome Metabólica, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil; National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Avenida Antônio Carlos, s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil.
Lucas José Sá Da FonsecaLaboratório de Reatividade Cardiovascular (LRC), Núcleo de Síndrome Metabólica, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil; National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Avenida Antônio Carlos, s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil.
Glaucevane Da Silva GuedesLaboratório de Reatividade Cardiovascular (LRC), Núcleo de Síndrome Metabólica, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil; National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Avenida Antônio Carlos, s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil; Faculdade de Nutrição (FANUT), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil.
Salete SmaniottoLaboratório de Biologia Celular, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil.
Luíza Antas RabeloLaboratório de Reatividade Cardiovascular (LRC), Núcleo de Síndrome Metabólica, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota, s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil; National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Avenida Antônio Carlos, s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil; Max Delbrück Center for Molecular Medicine, Robert-Rössle-Straße 10, 13125 Berlin, Germany.
National Institute of Science and Technology · IDMax Delbrück Center · DEUniversidade Federal de Alagoas · BRUniversidade Federal de Pernambuco · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) has been considered a novel component of the metabolic syndrome (MetS), with the oxidative stress participating in its progression. This study aimed to evaluate the metabolic profile in young and old mice with MetS, and the effects of apocynin and tempol on glycemic and lipid parameters. Young and old C57BL/6 mice with high fat diet- (HFD-) induced MetS received apocynin and tempol 50 mg·kg(-1)/day in their drinking water for 10 weeks. After HFD, the young group showed elevated fasting glucose, worsened lipid profile in plasma, steatosis, and hepatic lipid peroxidation. Nevertheless, the old group presented significant increase in fasting insulin levels, insulin resistance, plasma and hepatic lipid peroxidation, and pronounced steatosis. The hepatic superoxide dismutase and catalase activity did not differ between the groups. Tempol and apocynin seemed to prevent hepatic lipid deposition in both groups. Furthermore, apocynin improved glucose tolerance and insulin sensitivity in old mice. In summary, old mice are more susceptible to HFD-induced metabolic changes than their young counterparts. Also, the antioxidant therapy improved insulin sensitivity and glucose tolerance, and in addition, apocynin seemed to prevent the HFD-induced hepatic fat deposition, suggesting an important role of oxidative stress in the induction of NAFLD.

Indexed as

AgingDiet, High-FatAcetophenonesAnimalsAntioxidantsBlood GlucoseCatalaseCyclic N-OxidesDisease Models, AnimalGlucose Tolerance TestInsulinLipid PeroxidationLipidsLiverMetabolic SyndromeMiceAcetophenonesacetovanilloneAntioxidantsBlood GlucoseCatalaseCyclic N-OxidesInsulinLipidsSpin LabelsSuperoxide DismutasetempolTriglycerides

Identifiers

PMID27057272
PMCPMC4775807
OpenAlexW2277657693

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.