Evidence map›Paper›PMID 21041527›Full record

ArticleThe Journal of physiology2011

In obese Zucker rats, lipids accumulate in the heart despite normal mitochondrial content, morphology and long-chain fatty acid oxidation.

Graham P Holloway, Laelie A Snook, Robert J Harris, Jan F C Glatz, Joost J F P Luiken, Arend Bonen

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  6. Exogenous HAging and disease · 2020
    Article
  7. Article
  8. Article
  9. Diastolic dysfunction in prediabetic male rats: Role of mitochondrial oxidative stress.American journal of physiology. Heart and circulatory physiology · 2016
    Article
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  12. Review
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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 2 institutions in 2 countries.

Graham P HollowayHuman Health & Nutritional Sciences, University of Guelph, Guelph, Canada. ghollowa@uoguelph.ca
Laelie A Snook
Robert J Harris
Jan F C Glatz
Joost J F P Luiken
Arend Bonen
Maastricht University · NLUniversity of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to determine whether an increased rate of long-chain fatty acid (LCFA) transport and/or a reduction in mitochondrial oxidation contributes to lipid deposition in hearts, as lipid accumulation within cardiac muscle has been associated with heart failure. In hearts of lean and obese Zucker rats we examined: (a) triacylglycerol (TAG) and mitochondrial content and distribution using transmission electron microscopy (TEM), (b) LCFA oxidation in cardiac myocytes, and in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria, and (c) rates of LCFA transport into cardiac vesicles. Compared to lean rats, in obese Zucker rats, lipid droplet size was similar but there were more (P < 0.05) droplets, and TAG esterification rates and contents were markedly increased. TEM analyses and biochemical determinations showed that SS and IMF mitochondria in obese animals did not appear to be different in their appearance, area, density and number, nor in citrate synthase, β-hydroxy-acyl-CoA dehydrogenase and carnitine palmitoyl-transferase-I enzymatic activities, electron transport chain proteins, nor in their rates of LCFA oxidation either in cardiac myocytes or in isolated SS and IMF mitochondria (P > 0.05). In contrast, sarcolemmal plasma membrane fatty acid binding protein (FABPpm) and fatty acid translocase (FAT/CD36) protein and palmitate transport rates into cardiac vesicles were increased (P < 0.05; +50%) in obese animals. Collectively these data indicate that mitochondrial dysfunction in LCFA oxidation is not responsible for lipid accumulation in obese Zucker rat hearts. Rather, increased sarcolemmal LCFA transport proteins and rates of LCFA transport result in a greater number of lipid droplets within cardiac muscle.

Indexed as

3-Hydroxyacyl CoA DehydrogenasesAnimalsBiological TransportCarnitine O-PalmitoyltransferaseCD36 AntigensDisease Models, AnimalElectron Transport Chain Complex ProteinsEsterificationFatty Acid-Binding ProteinsFatty AcidsFemaleMicroscopy, Electron, TransmissionMitochondria, HeartMyocardiumObesityOxidation-Reduction3-Hydroxyacyl CoA DehydrogenasesCarnitine O-PalmitoyltransferaseCD36 AntigensCd36 protein, ratElectron Transport Chain Complex ProteinsFatty Acid-Binding ProteinsFatty AcidsPalmitic AcidTriglycerides

Identifiers

PMID21041527
PMCPMC3039267
OpenAlexW2033679770

What OpenQuestion 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 OpenQuestion graph.