Evidence map›Paper›PMID 24466104›Full record

ArticlePloS one2014

AT1 receptor blockade attenuates insulin resistance and myocardial remodeling in rats with diet-induced obesity.

Silvio A Oliveira-Junior, Paula F Martinez, Danielle M Guizoni, Dijon H S Campos, Tiago Fernandes, Edilamar M Oliveira, Marina P Okoshi, Katashi Okoshi, Carlos R Padovani, Antonio C Cicogna

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 55 citations in OpenAlex.

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  7. A Review of the Roles and Limitations of Noninvasive Imaging Methods for Investigating Cardiovascular Disease in Individuals with Obesity.Medical science monitor : international medical journal of experimental and clinical research · 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

10 authors at 3 institutions in 1 country.

Silvio A Oliveira-JuniorBotucatu Medical School, São Paulo State University, Botucatu, Brazil ; School of Physiotherapy, Federal University of Mato Grosso do Sul, Campo Grande, Brazil.
Paula F MartinezBotucatu Medical School, São Paulo State University, Botucatu, Brazil ; School of Physiotherapy, Federal University of Mato Grosso do Sul, Campo Grande, Brazil.
Danielle M GuizoniBotucatu Medical School, São Paulo State University, Botucatu, Brazil.
Dijon H S CamposBotucatu Medical School, São Paulo State University, Botucatu, Brazil.
Tiago FernandesSchool of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.
Edilamar M OliveiraSchool of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.
Marina P OkoshiBotucatu Medical School, São Paulo State University, Botucatu, Brazil.
Katashi OkoshiBotucatu Medical School, São Paulo State University, Botucatu, Brazil.
Carlos R PadovaniBotucatu Biosciences Institute, São Paulo State University, Botucatu, Brazil.
Antonio C CicognaBotucatu Medical School, São Paulo State University, Botucatu, Brazil.
Universidade Estadual Paulista (Unesp) · BRUniversidade de São Paulo · BRUniversidade Federal de Mato Grosso do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough obesity has been associated with metabolic and cardiac disturbances, the carrier mechanisms for these responses are poorly understood. This study analyzed whether angiotensin II blockade attenuates metabolic and cardiovascular disorders in rats with diet-induced obesity. MATERIAL AND

methodsWistar-Kyoto (n = 40) rats were subjected to control (C; 3.2 kcal/g) and hypercaloric diets (OB; 4.6 kcal/g) for 30 weeks. Subsequently, rats were distributed to four groups: C, CL, OB, and OBL. L groups received Losartan (30 mg/kg/day) for five weeks. After this period we performed in vivo glucose tolerance and insulin tolerance tests, and measured triacylglycerol, insulin, angiotensin-converting enzyme activity (ACE), and leptin levels. Cardiovascular analyzes included systolic blood pressure (SBP), echocardiography, myocardial morphometric study, myosin heavy chain composition, and measurements of myocardial protein levels of angiotensin, extracellular signal-regulated (ERK1/2), c-Jun amino-terminal kinases (JNK), insulin receptor subunit β (βIR), and phosphatidylinositol 3-kinase (PI3K) by Western Blot.

resultsGlucose metabolism, insulin, lipid, and ACE activity disorders observed with obesity were minimized by Losartan. Moreover, obesity was associated with increased SBP, myocardial hypertrophy, interstitial fibrosis and improved systolic performance; these effects were also minimized with Losartan. On a molecular level, OB exhibited higher ERK, Tyr-phosphorylated βIR, and PI3K expression, and reduced myocardial angiotensin and JNK expression. ERK and JNK expression were regulated in the presence of Losartan, while angiotensin, Tyr-βRI, total and Tyr-phosphorylated PI3K expression were elevated in the OBL group.

conclusionAngiotensin II blockade with Losartan attenuates obesity-induced metabolic and cardiovascular changes.

Indexed as

Insulin ResistanceVentricular RemodelingAngiotensin II Type 1 Receptor BlockersAngiotensinsAnimalsBlood GlucoseClass Ia Phosphatidylinositol 3-KinaseEnergy IntakeLosartanMaleMAP Kinase Signaling SystemMyocardiumMyosin Heavy ChainsObesityRatsRats, Inbred WKYAngiotensin II Type 1 Receptor BlockersAngiotensinsBlood GlucoseClass Ia Phosphatidylinositol 3-KinaseLosartanMyosin Heavy ChainsReceptor, Angiotensin, Type 1Receptor, Insulin

Identifiers

PMID24466104
PMCPMC3900554
OpenAlexW1998046994

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.