Evidence map›Paper›PMID 8729132›Full record

ReviewLipids1996

Arachidonic acid maldistribution in obesity.

S D Phinney

Abstract readReview
PubMed Publisher
In one paragraph

Review in Lipids, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

1 author at 1 institution in 1 country.

S D PhinneyDepartment of Internal Medicine, University of California, Davis 95616, USA.
University of California, Davis · US

Funding

VITAMINS, AMINO ACIDS, AND RELATED PRODUCTS CORE LABORATORYP30DK035747 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI HALSTED, CHARLES HOPKINSON · 1986 to 2005
$4.7M
NIDDK NIH HHS DK35747
6 · The paper itself

Abstract

Arachidonic acid is an important regulator of cellular function via its effects on the physical properties of membranes, in its free form, or as a substrate for eicosanoids. Dietary studies indicate that its production is regulated, but the mechanisms of this regulation and factors influencing arachidonate distribution from the site of production remain to be determined. In particular, whether there is a nonoxidative fate for arachidonate once it has been released from phospholipid has yet to be determined. Variations in the arachidonate content of serum, liver, and muscle lipid fractions have been correlated with alterations in lipogenesis and insulin action, implying a role for arachidonate in fuel partitioning. Evidence for this mechanism acting systemically has been found in genetic models of obesity in rodents and also in humans. This review proposes that variation in the distribution of arachidonate between phospholipid and cholesteryl ester fractions participates in the abnormal fuel partitioning associated with some forms of genetic obesity.

Indexed as

AnimalsArachidonic AcidDietary Fats, UnsaturatedFatty Acids, Omega-3Fatty Acids, Omega-6Fatty Acids, UnsaturatedHumansLipid MetabolismLipidsModels, GeneticObesityRatsRats, ZuckerArachidonic AcidDietary Fats, UnsaturatedFatty Acids, Omega-3Fatty Acids, Omega-6Fatty Acids, UnsaturatedLipids

Identifiers

PMID8729132
OpenAlexW2082104703

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.