Evidence map›Paper›PMID 20529848›Full record

ArticleThe Journal of biological chemistry2010

Adaptation of myocardial substrate metabolism to a ketogenic nutrient environment.

Anna E Wentz, D André d'Avignon, Mary L Weber, David G Cotter, Jason M Doherty, Robnet Kerns, Rakesh Nagarajan, Naveen Reddy, Nandakumar Sambandam, Peter A Crawford

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025
    Review
  9. Article
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  11. Article
  12. Review
  13. Review
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  16. Article
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31 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Anna E WentzDepartment of Medicine, Washington University, St Louis, Missouri 63108, USA.
D André d'Avignon
Mary L Weber
David G Cotter
Jason M Doherty
Robnet Kerns
Rakesh Nagarajan
Naveen Reddy
Nandakumar Sambandam
Peter A Crawford
Washington University in St. Louis · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Irfan J Lodhi · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
Gnotobiotic mouse models/microbial regulation of intestinal injuryK08DK073282 · NIDDK · WASHINGTON UNIVERSITY · PI CRAWFORD, PETER A · 2006 to 2010
$600k
NIDDK NIH HHS DK020579NIDDK NIH HHS DK073282NIDDK NIH HHS K08 DK073282NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P60 DK020579
6 · The paper itself

Abstract

Heart muscle is metabolically versatile, converting energy stored in fatty acids, glucose, lactate, amino acids, and ketone bodies. Here, we use mouse models in ketotic nutritional states (24 h of fasting and a very low carbohydrate ketogenic diet) to demonstrate that heart muscle engages a metabolic response that limits ketone body utilization. Pathway reconstruction from microarray data sets, gene expression analysis, protein immunoblotting, and immunohistochemical analysis of myocardial tissue from nutritionally modified mouse models reveal that ketotic states promote transcriptional suppression of the key ketolytic enzyme, succinyl-CoA:3-oxoacid CoA transferase (SCOT; encoded by Oxct1), as well as peroxisome proliferator-activated receptor alpha-dependent induction of the key ketogenic enzyme HMGCS2. Consistent with reduction of SCOT, NMR profiling demonstrates that maintenance on a ketogenic diet causes a 25% reduction of myocardial (13)C enrichment of glutamate when (13)C-labeled ketone bodies are delivered in vivo or ex vivo, indicating reduced procession of ketones through oxidative metabolism. Accordingly, unmetabolized substrate concentrations are higher within the hearts of ketogenic diet-fed mice challenged with ketones compared with those of chow-fed controls. Furthermore, reduced ketone body oxidation correlates with failure of ketone bodies to inhibit fatty acid oxidation. These results indicate that ketotic nutrient environments engage mechanisms that curtail ketolytic capacity, controlling the utilization of ketone bodies in ketotic states.

Indexed as

AnimalsCarbon IsotopesCoenzyme A-TransferasesImmunohistochemistryKetone BodiesKetonesMaleMiceMice, Inbred C57BLMice, TransgenicModels, BiologicalMyocardiumMyocytes, CardiacPeroxisome Proliferator-Activated ReceptorsRats3-ketoacid CoA-transferaseCarbon IsotopesCoenzyme A-TransferasesKetone BodiesKetonesPeroxisome Proliferator-Activated Receptors

Identifiers

PMID20529848
PMCPMC2915681
OpenAlexW1964394222

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.