Evidence map›Paper›PMID 19892241›Full record

ArticleJournal of the American College of Cardiology2009

Substrate-specific derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart.

Ethan J Anderson, Alan P Kypson, Evelio Rodriguez, Curtis A Anderson, Eric J Lehr, P Darrell Neufer

Abstract read
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In one paragraph

Article in Journal of the American College of Cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 3 pooled it
8.2field-weighted citation impact, top 2% 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

252 citing papers in PubMed, 3 syntheses or guidelines pooled it, 422 citations in OpenAlex.

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  20. The heart of diabetes: unraveling metabolic drivers of cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2025
    Review

192 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Ethan J AndersonDepartment of Cardiovascular Sciences and East Carolina Heart Institute, East Carolina University, Greenville, North Carolina 27835, USA. andersonet@ecu.edu.
Alan P Kypson
Evelio Rodriguez
Curtis A Anderson
Eric J Lehr
P Darrell Neufer
East Carolina University · US

Funding

Linking Mitochondrial Bioenergetics to Muscle Insulin SensitivityR01DK074825 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2009 to 2013
$1.6M
Mitochondrial Bioenergetics and Etiology of Insulin ResistanceR01DK073488 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2007 to 2010
$1.2M
NIDDK NIH HHS DK073488NIDDK NIH HHS DK074825NIDDK NIH HHS R01 DK073488NIDDK NIH HHS R01 DK074825
6 · The paper itself

Abstract

objectivesThe aim of this study was to determine the impact of diabetes on oxidant balance and mitochondrial metabolism of carbohydrate- and lipid-based substrates in myocardium of type 2 diabetic patients.

backgroundHeart failure represents a major cause of death among diabetic patients. It has been proposed that derangements in cardiac metabolism and oxidative stress may underlie the progression of this comorbidity, but scarce evidence exists in support of this mechanism in humans.

methodsMitochondrial oxygen (O(2)) consumption and hydrogen peroxide (H(2)O(2)) emission were measured in permeabilized myofibers prepared from samples of the right atrial appendage obtained from nondiabetic (n = 13) and diabetic (n = 11) patients undergoing nonemergent coronary artery bypass graft surgery.

resultsMitochondria in atrial tissue of type 2 diabetic individuals show a sharply decreased capacity for glutamate and fatty acid-supported respiration, in addition to an increased content of myocardial triglycerides, as compared to nondiabetic patients. Furthermore, diabetic patients show an increased mitochondrial H(2)O(2) emission during oxidation of carbohydrate- and lipid-based substrates, depleted glutathione, and evidence of persistent oxidative stress in their atrial tissue.

conclusionsThese findings are the first to directly investigate the effects of type 2 diabetes on a panoply of mitochondrial functions in the human myocardium using cellular and molecular approaches, and they show that mitochondria in diabetic human hearts have specific impairments in maximal capacity to oxidize fatty acids and glutamate, yet increased mitochondrial H(2)O(2) emission, providing insight into the role of mitochondrial dysfunction and oxidative stress in the pathogenesis of heart failure in diabetic patients.

Indexed as

Oxidative StressAdenosine DiphosphateAdultCell RespirationCitric Acid CycleDiabetes Mellitus, Type 2Fatty AcidsFemaleGlutamic AcidGlutathioneHeart AtriaHeat-Shock ProteinsHumansHydrogen PeroxideKineticsMaleAdenosine DiphosphateFatty AcidsGlutamic AcidGlutathioneHeat-Shock ProteinsHydrogen PeroxidePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR alphaPPARGC1A protein, humanTranscription FactorsTriglycerides

Identifiers

PMID19892241
PMCPMC2800130
OpenAlexW2077261489

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.