Evidence map›Paper›PMID 26567194›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2015

Potential for dietary ω-3 fatty acids to prevent nonalcoholic fatty liver disease and reduce the risk of primary liver cancer.

Donald B Jump, Christopher M Depner, Sasmita Tripathy, Kelli A Lytle

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Donald B JumpNutrition Program, School of Biological and Population Health Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR donald.jump@oregonstate.edu.
Christopher M DepnerNutrition Program, School of Biological and Population Health Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR.
Sasmita TripathyNutrition Program, School of Biological and Population Health Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR.
Kelli A LytleNutrition Program, School of Biological and Population Health Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR.
Oregon State University · US

Funding

PUFA Synthesis and the Control of Hepatic MetabolismR01DK094600 · NIDDK · OREGON STATE UNIVERSITY · PI JUMP, DONALD B · 2012 to 2015
$1.2M
NIDDK NIH HHS DK094600NIDDK NIH HHS DK 43220NIDDK NIH HHS R01 DK094600
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) has increased in parallel with central obesity, and its prevalence is anticipated to increase as the obesity epidemic remains unabated. NAFLD is now the most common cause of chronic liver disease in developed countries and is defined as excessive lipid accumulation in the liver, that is, hepatosteatosis. NAFLD ranges in severity from benign fatty liver to nonalcoholic steatohepatitis (NASH), and NASH is characterized by hepatic injury, inflammation, oxidative stress, and fibrosis. NASH can progress to cirrhosis, and cirrhosis is a risk factor for primary hepatocellular carcinoma (HCC). The prevention of NASH will lower the risk of cirrhosis and NASH-associated HCC. Our studies have focused on NASH prevention. We developed a model of NASH by using mice with the LDL cholesterol receptor gene ablated fed the Western diet (WD). The WD induces a NASH phenotype in these mice that is similar to that seen in humans and includes robust induction of hepatic steatosis, inflammation, oxidative stress, and fibrosis. With the use of transcriptomic, lipidomic, and metabolomic approaches, we examined the capacity of 2 dietary ω-3 (n-3) polyunsaturated fatty acids, eicosapentaenoic acid (20:5ω-3; EPA) and docosahexaenoic acid (22:6ω-3; DHA), to prevent WD-induced NASH. Dietary DHA was superior to EPA at attenuating WD-induced changes in plasma lipids and hepatic injury and at reversing WD effects on hepatic metabolism, oxidative stress, and fibrosis. The outcome of these studies suggests that DHA may be useful in preventing NASH and reducing the risk of HCC.

Indexed as

AnimalsDietary Fats, UnsaturatedDiet, WesternDisease Models, AnimalDocosahexaenoic AcidsEicosapentaenoic AcidFatty Acids, Omega-3Fatty LiverHepatitisHumansLiver CirrhosisLiver NeoplasmsMiceMice, KnockoutMice, ObeseNon-alcoholic Fatty Liver DiseaseDietary Fats, UnsaturatedDocosahexaenoic AcidsEicosapentaenoic AcidFatty Acids, Omega-3Receptors, LDLfatty liver diseasefibrosisinflammationliver cancermetabolomicsoxidative stressω-3 PUFAs

Identifiers

PMID26567194
PMCPMC4642422
OpenAlexW2175085616

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.