Evidence map›Paper›PMID 19937697›Full record

ArticleHepatology (Baltimore, Md.)2009

The plasma lipidomic signature of nonalcoholic steatohepatitis.

Puneet Puri, Michelle M Wiest, Onpan Cheung, Faridoddin Mirshahi, Carol Sargeant, Hae-Ki Min, Melissa J Contos, Richard K Sterling, Michael Fuchs, Huiping Zhou and 2 more

Abstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 347 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
347citing papers in PubMed, 2 pooled it
15.6field-weighted citation impact, top 1% 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

347 citing papers in PubMed, 2 syntheses or guidelines pooled it, 643 citations in OpenAlex.

  1. Biomarker discovery in NAFLD: insights from metabolomics and vote counting meta-analysis.Metabolomics : Official journal of the Metabolomic Society · 2025
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287 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Puneet PuriDivision of Gastroenterology, Department of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA, USA
Michelle M Wiest
Onpan Cheung
Faridoddin Mirshahi
Carol Sargeant
Hae-Ki Min
Melissa J Contos
Richard K Sterling
Michael Fuchs
Huiping Zhou
Steven M Watkins
Arun J Sanyal
Virginia Commonwealth University Medical Center · USVirginia Commonwealth University · US

Funding

Training Grant in Digestive Diseases and Liver DiseasesT32DK007150 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 1986 to 2017
$4.2M
Molecular Determinants of Disease Progression in Nonalcoholic SteatohepatitisR01DK081410 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 2009 to 2013
$1.7M
Studies of Mechanisms and Treatment of Liver DiseasesK24DK002755 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 1999 to 2008
$1.2M
NIDDK NIH HHS K24 DK002755NIDDK NIH HHS K24 DK 02755-06NIDDK NIH HHS R01 DK081410NIDDK NIH HHS T32 DK007150NIDDK NIH HHS T32 DK 07150-31PHS HHS R01 56331-05
6 · The paper itself

Abstract

unlabelledSpecific alterations in hepatic lipid composition characterize the spectrum of nonalcoholic fatty liver disease (NAFLD), which extends from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH). However, the plasma lipidome of NAFLD and whether NASH has a distinct plasma lipidomic signature are unknown. A comprehensive analysis of plasma lipids and eicosanoid metabolites quantified by mass spectrometry was performed in NAFL (n = 25) and NASH (n = 50) subjects and compared with lean normal controls (n = 50). The key findings include significantly increased total plasma monounsaturated fatty acids driven by palmitoleic (16:1 n7) and oleic (18:1 n9) acids content (P < 0.01 for both acids in both NAFL and NASH). The levels of palmitoleic acid, oleic acid, and palmitoleic acid to palmitic acid (16:0) ratio were significantly increased in NAFLD across multiple lipid classes. Linoleic acid (8:2n6) was decreased (P < 0.05), with a concomitant increase in gamma-linolenic (18:3n6) and dihomo gamma-linolenic (20:3n6) acids in both NAFL and NASH (P < 0.001 for most lipid classes). The docosahexanoic acid (22:6 n3) to docosapentenoic acid (22:5n3) ratio was significantly decreased within phosphatidylcholine (PC), and phosphatidylethanolamine (PE) pools, which was most marked in NASH subjects (P < 0.01 for PC and P < 0.001 for PE). The total plasmalogen levels were significantly decreased in NASH compared with controls (P < 0.05). A stepwise increase in lipoxygenase (LOX) metabolites 5(S)-hydroxyeicosatetraenoic acid (5-HETE), 8-HETE, and 15-HETE characterized progression from normal to NAFL to NASH. The level of 11-HETE, a nonenzymatic oxidation product of arachidonic (20:4) acid, was significantly increased in NASH only.

conclusionsAlthough increased lipogenesis, desaturases, and LOX activities characterize NAFL and NASH, impaired peroxisomal polyunsaturated fatty acid (PUFA) metabolism and nonenzymatic oxidation is associated with progression to NASH.

Indexed as

Arachidonic AcidDiglyceridesFatty Acids, NonesterifiedFatty Acids, UnsaturatedFatty LiverFemaleHumansLipidsLipogenesisMaleMetabolomicsPhospholipidsTriglyceridesArachidonic AcidDiglyceridesFatty Acids, NonesterifiedFatty Acids, UnsaturatedLipidsPhospholipidsTriglycerides

Identifiers

PMID19937697
PMCPMC5031239
OpenAlexW1998323589

What OpenQuestion holds

Textmetadata
LicenceTDM
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.