Evidence map›Paper›PMID 22542451›Full record

ArticleJournal of molecular and cellular cardiology2012

Normalizing the metabolic phenotype after myocardial infarction: impact of subchronic high fat feeding.

Jessica M Berthiaume, Martin E Young, Xiaoqin Chen, Tracy A McElfresh, Xin Yu, Margaret P Chandler

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Functional resilience of C57BL/6J mouse heart to dietary fat overload.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Re-balancing cellular energy substrate metabolism to mend the failing heart.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Metabolic Origins of Heart Failure.JACC. Basic to translational science · 2017
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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 2 institutions in 1 country.

Jessica M BerthiaumeDept of Physiology & Biophysics, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106-4970, USA.
Martin E Young
Xiaoqin Chen
Tracy A McElfresh
Xin Yu
Margaret P Chandler
Case Western Reserve University · USUniversity of Alabama at Birmingham · US

Funding

Effects of Dietary Fat on Contractile and Mitochondrial Function in Heart FailureR01HL081857 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI CHANDLER, MARGARET P · 2006 to 2010
$2.2M
NHLBI NIH HHS HL081857NHLBI NIH HHS R01 HL081857
6 · The paper itself

Abstract

The normal heart relies primarily on the oxidation of fatty acids (FA) for ATP production, whereas during heart failure (HF) glucose utilization increases, implying pathological changes to cardiac energy metabolism. Despite the noted lipotoxic effects of elevating FA, our work has demonstrated a cardioprotective effect of a high fat diet (SAT) when fed after myocardial infarction (MI), as compared to normal chow (NC) fed cohorts. This data has suggested a mechanistic link to energy metabolism. The goal of this study was to determine the impact of SAT on the metabolic phenotype of the heart after MI. Male Wistar rats underwent coronary ligation surgery (MI) and were evaluated after 8 weeks of SAT. Induction of MI was verified by echocardiography. LV function assessed by in vivo hemodynamic measurements revealed improvements in the MI-SAT group as compared to MI-NC. Perfused working hearts revealed a decrease in cardiac work in MI-NC that was improved in MI-SAT. Glucose oxidation was increased and FA oxidation decreased in MI-NC compared to shams suggesting an alteration in the metabolic profile that was ameliorated by SAT. (31)P NMR analysis of Langendorff perfused hearts revealed no differences in PCr:ATP indicating no overt energy deficit in MI groups. Phospho-PDH and PDK(4) were increased in MI-SAT, consistent with a shift towards fatty acid oxidation (FAO). Overall, these results support the hypothesis that SAT post-infarction promotes a normal metabolic phenotype that may serve a cardioprotective role in the injured heart.

Indexed as

Diet, High-FatMetabolomeAdenosine TriphosphateAnimalsDisease Models, AnimalEchocardiographyEnergy MetabolismHemodynamicsMaleMyocardial InfarctionMyocardiumPhenotypePhosphocreatinePhosphorylationProtein KinasesPyruvate Dehydrogenase ComplexAdenosine TriphosphatePhosphocreatineProtein KinasesPyruvate Dehydrogenase Complexpyruvate dehydrogenase kinase 4

Identifiers

PMID22542451
PMCPMC3372615
OpenAlexW2089846356

What OpenQuestion holds

Textmetadata
LicenceTDM
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.