Evidence map›Paper›PMID 21701073›Full record

ArticleThe Journal of clinical investigation2011

Adenosine: front and center in linking nutrition and metabolism to neuronal activity.

Robert W Greene

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Preventive effects of ketone ester BD-AcAcDiving and hyperbaric medicine · 2018
    Article
  4. Ketotic hypercalcemia: a case series and description of a novel entity.The Journal of clinical endocrinology and metabolism · 2014
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Robert W GreeneDepartment of Psychiatry, University of Texas Southwestern Medical Center and Dallas VA Medical Center, Dallas, Texas 75390, USA. robertw.greene@utsouthwestern.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many individuals with epilepsy benefit from consuming a ketogenic diet, which is similar to the more commonly known Atkins diet. The underlying molecular reason for this has not been determined. However, in this issue of the JCI, Masino et al. have elucidated the mechanism responsible for the antiepileptic effects of the ketogenic diet in mice. The diet is shown to decrease expression of the enzyme adenosine kinase (Adk), which is responsible for clearing the endogenous antiepileptic agent adenosine (Ado) from the extracellular CNS space. Decreased expression of Adk results in increased extracellular Ado, activation of inhibitory Ado A1 receptors, and decreased seizure generation, the desired therapeutic effect. The authors' work serves to emphasize the importance of controlling Adk expression, not only as the mechanism of action of the ketogenic diet, but also as a potential target of future therapies.

Indexed as

Diet, KetogenicAnimalsEpilepsyHumansReceptor, Adenosine A1SeizuresReceptor, Adenosine A1

Identifiers

PMID21701073
PMCPMC3223847

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.