Evidence map›Paper›PMID 29118818›Full record

ArticleNutrition & metabolism2017

Folic acid prevents cardiac dysfunction and reduces myocardial fibrosis in a mouse model of high-fat diet-induced obesity.

Wei Li, Renqiao Tang, Shengrong Ouyang, Feifei Ma, Zhuo Liu, Jianxin Wu

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 49 citations in OpenAlex.

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  16. Treatment of Oxidative Stress with Exosomes in Myocardial Ischemia.International journal of molecular sciences · 2021
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  17. Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases.Frontiers in cell and developmental biology · 2021
    Review
  18. Correlation Analysis BetweenFrontiers in oncology · 2021
    Article
  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

6 authors at 3 institutions in 1 country.

Wei LiGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Renqiao TangGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Shengrong OuyangGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Feifei MaGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Zhuo LiuGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Jianxin WuGraduate School of Peking Union Medical College, NO. 9, Dongdansantiao, Dongcheng District, Beijing, 100730 China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CNCapital Institute of Pediatrics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFolic acid (FA) is an antioxidant that can reduce reactive oxygen species generation and can blunt cardiac dysfunction during ischemia. We hypothesized that FA supplementation prevents cardiac fibrosis and cardiac dysfunction induced by obesity.

methodsSix-week-old C57BL6/J mice were fed a high-fat diet (HFD), normal diet (ND), or an HFD supplemented with folic acid (FAD) for 14 weeks. Cardiac function was measured using a transthoracic echocardiographic exam. Phenotypic analysis included measurements of body and heart weight, blood glucose and tissue homocysteine (Hcy) content, and heart oxidative stress status.

resultsHFD consumption elevated fasting blood glucose levels and caused obesity and heart enlargement. FA supplementation in HFD-fed mice resulted in reduced fasting blood glucose, heart weight, and heart tissue Hcy content. We also observed a significant cardiac systolic dysfunction when mice were subjected to HFD feeding as indicated by a reduction in the left ventricular ejection fraction and fractional shortening. However, FAD treatment improved cardiac function. FA supplementation protected against cardiac fibrosis induced by HFD. In addition, HFD increased malondialdehyde concentration of the heart tissue and reduced the levels of antioxidant enzyme, glutathione, and catalase. HFD consumption induced myocardial oxidant stress with amelioration by FA treatment.

conclusionFA supplementation significantly lowers blood glucose levels and heart tissue Hcy content and reverses cardiac dysfunction induced by HFD in mice. These functional improvements of the heart may be mediated by the alleviation of oxidative stress and myocardial fibrosis.

Indexed as

Cardiac functionFolic acidHigh-fat dietMyocardial fibrosisOxidative stress

Identifiers

PMID29118818
PMCPMC5668988
OpenAlexW2766703051

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.