Evidence mapPaperPMID 25564432Full record

ArticleEuropean journal of nutrition2016

Early developmental exposure to high fructose intake in rats with NaCl stimulation causes cardiac damage.

I C Araujo, R P Andrade, F Santos, E S Soares, R Yokota, C Mostarda, P Fiorino, K De Angelis, M C Irigoyen, M Morris and 1 more

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In one paragraph

Article in European journal of nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.7field-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

5 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Article
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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

11 authors at 6 institutions in 2 countries.

I C AraujoTranslational Medicine Division, Department of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. araujo.iara@hotmail.com.
R P AndradeRenal, Cardiovascular and Metabolic Physiopharmacology Laboratory, Health and Biological Science Center, Mackenzie University, Rua da Consolacao, 930, São Paulo, SP, 01302-907, Brazil. romario.pan@hotmail.com.
F SantosHypertension Unit, Heart Institute (InCor), School of Medicine, University of São Paulo (FMUSP), Avenida Doutor Eneas de Carvalho Aguiar, 44 - Cerqueira Cesar, São Paulo, SP, 05403-900, Brazil. fernandostos@ig.com.br.
E S SoaresRenal, Cardiovascular and Metabolic Physiopharmacology Laboratory, Health and Biological Science Center, Mackenzie University, Rua da Consolacao, 930, São Paulo, SP, 01302-907, Brazil. eli.sinais@gmail.com.
R YokotaTranslational Medicine Division, Department of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. yokota_rodrigo@hotmail.com.
C MostardaFederal Univeristy of Maranhao- UFMA, São Luis, MA, Brazil. cristiano.mostarda@gmail.com.
P FiorinoRenal, Cardiovascular and Metabolic Physiopharmacology Laboratory, Health and Biological Science Center, Mackenzie University, Rua da Consolacao, 930, São Paulo, SP, 01302-907, Brazil. patriciafiorino@mackenzie.br.
K De AngelisTranslational Physiology Laboratory, Universidade Nove de Julho (UNINOVE), Rua Vergueiro 235/249, Liberdade, São Paulo, SP, 01504-001, Brazil. prof.kangelis@uninove.br.
M C IrigoyenHypertension Unit, Heart Institute (InCor), School of Medicine, University of São Paulo (FMUSP), Avenida Doutor Eneas de Carvalho Aguiar, 44 - Cerqueira Cesar, São Paulo, SP, 05403-900, Brazil. maria.irigoyen@incor.usp.br.
M MorrisCollege of Osteopathic Medicine, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL, 33328-2018, USA. mmorris1@nova.edu.
V FarahTranslational Medicine Division, Department of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. verafarah@hotmail.com.
Universidade Presbiteriana Mackenzie · BRUniversidade de São Paulo · BRUniversidade Federal de São Paulo · BRNova Southeastern University · USUniversidade Federal do Maranhão · BRUniversidade Nove de Julho · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMetabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood.

methodsMale Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10%, F), NaCl consumption (salt 1% for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol.

resultsEnergy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 ± 9 bpm) compared with the C group (410 ± 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26%, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group.

conclusionsData suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.

Indexed as

AnimalsArterial PressureBlood GlucoseBlood PressureCardiovascular DiseasesCardiovascular SystemCholesterol, HDLCholesterol, LDLDiabetes Mellitus, Type 2FructoseGlucose IntoleranceGlucose Tolerance TestHeartHeart RateInsulinInsulin ResistanceBlood GlucoseCholesterol, HDLCholesterol, LDLFructoseInsulinSodium Chloride, DietaryTriglyceridesCardiovascular riskFructoseMetabolic syndromeNaClRenin angiotensin system

Identifiers

PMID25564432
OpenAlexW2112955706

What Socratic 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 Socratic graph.