Evidence map›Paper›PMID 23233542›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

Successful adaptation to ketosis by mice with tissue-specific deficiency of ketone body oxidation.

David G Cotter, Rebecca C Schugar, Anna E Wentz, D André d'Avignon, Peter A Crawford

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-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

39 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Dietary restriction reprograms CD8Nature metabolism · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Ketolysis drives CD8Immunity · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Regulation of adult stem cell function by ketone bodies.Frontiers in cell and developmental biology · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Functional loss of ketogenesis in odontocete cetaceans.The Journal of experimental biology · 2021
    Article
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

5 authors at 1 institution in 1 country.

David G CotterDivision of Cardiology, Dept. of Medicine, Washington Univ. School of Medicine, St. Louis, MO 63110, USA.
Rebecca C Schugar
Anna E Wentz
D André d'Avignon
Peter A Crawford
Washington University in St. Louis · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
KETONE BODY METABOLISM AND INTEGRATED METABOLIC HOMEOSTASISR01DK091538 · NIDDK · WASHINGTON UNIVERSITY · PI CRAWFORD, PETER A · 2011 to 2024
$6.2M
NHLBI NIH HHS HL-007275NHLBI NIH HHS HL-007873NIDDK NIH HHS DK-020579NIDDK NIH HHS DK-091538NIDDK NIH HHS P30 DK020579NIDDK NIH HHS R01 DK091538
6 · The paper itself

Abstract

During states of low carbohydrate intake, mammalian ketone body metabolism transfers energy substrates originally derived from fatty acyl chains within the liver to extrahepatic organs. We previously demonstrated that the mitochondrial enzyme coenzyme A (CoA) transferase [succinyl-CoA:3-oxoacid CoA transferase (SCOT), encoded by nuclear Oxct1] is required for oxidation of ketone bodies and that germline SCOT-knockout (KO) mice die within 48 h of birth because of hyperketonemic hypoglycemia. Here, we use novel transgenic and tissue-specific SCOT-KO mice to demonstrate that ketone bodies do not serve an obligate energetic role within highly ketolytic tissues during the ketogenic neonatal period or during starvation in the adult. Although transgene-mediated restoration of myocardial CoA transferase in germline SCOT-KO mice is insufficient to prevent lethal hyperketonemic hypoglycemia in the neonatal period, mice lacking CoA transferase selectively within neurons, cardiomyocytes, or skeletal myocytes are all viable as neonates. Like germline SCOT-KO neonatal mice, neonatal mice with neuronal CoA transferase deficiency exhibit increased cerebral glycolysis and glucose oxidation, and, while these neonatal mice exhibit modest hyperketonemia, they do not develop hypoglycemia. As adults, tissue-specific SCOT-KO mice tolerate starvation, exhibiting only modestly increased hyperketonemia. Finally, metabolic analysis of adult germline Oxct1(+/-) mice demonstrates that global diminution of ketone body oxidation yields hyperketonemia, but hypoglycemia emerges only during a protracted state of low carbohydrate intake. Together, these data suggest that, at the tissue level, ketone bodies are not a required energy substrate in the newborn period or during starvation, but rather that integrated ketone body metabolism mediates adaptation to ketogenic nutrient states.

Indexed as

AgingAdaptation, PhysiologicalAnimalsAnimals, NewbornCaloric RestrictionCoenzyme A-TransferasesHeterozygoteHypoglycemiaKetone BodiesKetosisMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalMyocytes, Cardiac3-ketoacid CoA-transferaseCoenzyme A-TransferasesKetone BodiesNerve Tissue Proteins

Identifiers

PMID23233542
PMCPMC3566508
OpenAlexW2147718544

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.