Evidence map›Paper›PMID 28381467›Full record

ArticleJournal of the American Heart Association2017

Hepatic Ketogenesis Induced by Middle Cerebral Artery Occlusion in Mice.

Konrad Koch, Dirk Berressem, Jan Konietzka, Anna Thinnes, Gunter P Eckert, Jochen Klein

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Blood and Brain Metabolites after Cerebral Ischemia.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. 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

6 authors at 1 institution in 1 country.

Konrad KochDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany.
Dirk BerressemDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany.
Jan KonietzkaDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany.
Anna ThinnesDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany.
Gunter P EckertDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany.
Jochen KleinDepartment of Pharmacology, FB 14, Goethe University, Frankfurt, Germany klein@em.uni-frankfurt.de.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKetone bodies are known to substitute for glucose as brain fuel when glucose availability is low. Ketogenic diets have been described as neuroprotective. Similar data have been reported for triheptanoin, a fatty oil and anaplerotic compound. In this study, we monitored the changes of energy metabolites in liver, blood, and brain after transient brain ischemia to test for ketone body formation induced by experimental stroke. METHODS AND

resultsMice were fed a standard carbohydrate-rich diet or 2 fat-rich diets, 1 enriched in triheptanoin and 1 in soybean oil. Stroke was induced in mice by middle cerebral artery occlusion for 90 minutes, followed by reperfusion. Mice were sacrificed, and blood plasma and liver and brain homogenates were obtained. In 1 experiment, microdialysis was performed. Metabolites (eg glucose, β-hydroxybutyrate, citrate, succinate) were determined by gas chromatography-mass spectrometry. After 90 minutes of brain ischemia, β-hydroxybutyrate levels were dramatically increased in liver, blood, and brain microdialysate and brain homogenate, but only in mice fed fat-rich diets. Glucose levels were changed in the opposite manner in blood and brain. Reperfusion decreased β-hydroxybutyrate and increased glucose within 60 minutes. Stroke-induced ketogenesis was blocked by propranolol, a β-receptor antagonist. Citrate and succinate were moderately increased by fat-rich diets and unchanged after stroke.

conclusionsWe conclude that brain ischemia induces the formation of β-hydroxybutyrate (ketogenesis) in the liver and the consumption of β-hydroxybutyrate in the brain. This effect seems to be mediated by β-adrenergic receptors.

Indexed as

3-Hydroxybutyric AcidAdrenergic beta-AntagonistsAnimalsBrainBrain IschemiaCitric AcidDiet, Carbohydrate LoadingDiet, High-FatDisease Models, AnimalFemaleGas Chromatography-Mass SpectrometryGlucoseInfarction, Middle Cerebral ArteryKetone BodiesLiverMice3-Hydroxybutyric AcidAdrenergic beta-AntagonistsCitric AcidGlucoseKetone BodiesPropranololSoybean OilSuccinic AcidTriglyceridestriheptanoincerebral ischemiacitrateglucoseketone bodieslactatemiddle cerebral artery occlusionmousesuccinateβ‐hydroxybutyrate

Identifiers

PMID28381467
PMCPMC5533036
OpenAlexW2604517254

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.