Evidence map›Paper›PMID 26282529›Full record

ArticleThe Proceedings of the Nutrition Society2016

Impact of dietary fat on the development of non-alcoholic fatty liver disease in Ldlr-/- mice.

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

Open access · bronzeAbstract read
In one paragraph

Article in The Proceedings of the Nutrition Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Vitamin DImmunity, inflammation and disease · 2017
    Article
  16. Article
  17. Liver-specific loss of Perilipin 2 alleviates diet-induced hepatic steatosis, inflammation, and fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Article
  18. 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

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 Oregon, 97331,USA.
Christopher M DepnerNutrition Program,School of Biological and Population Health Sciences,Linus Pauling Institute,Oregon State University,Corvallis Oregon, 97331,USA.
Sasmita TripathyNutrition Program,School of Biological and Population Health Sciences,Linus Pauling Institute,Oregon State University,Corvallis Oregon, 97331,USA.
Kelli A LytleNutrition Program,School of Biological and Population Health Sciences,Linus Pauling Institute,Oregon State University,Corvallis Oregon, 97331,USA.
Oregon State University · US

Funding

DIETARY FAT REGULATION OF HEPATIC GENE EXPRESSIONR01DK043220 · NIDDK · OREGON STATE UNIVERSITY · PI JUMP, DONALD B · 1991 to 2009
$2.7M
PUFA Synthesis and the Control of Hepatic MetabolismR01DK094600 · NIDDK · OREGON STATE UNIVERSITY · PI JUMP, DONALD B · 2012 to 2015
$1.2M
NIDDK NIH HHS R01 DK043220NIDDK NIH HHS R01 DK094600
6 · The paper itself

Abstract

The prevalence of non-alcoholic fatty liver disease (NAFLD) has increased in parallel with central obesity and is now the most common chronic liver disease in developed countries. NAFLD is defined as excessive accumulation of lipid in the liver, i.e. hepatosteatosis. The severity of NAFLD ranges from simple fatty liver (steatosis) to non-alcoholic steatohepatitis (NASH). Simple steatosis is relatively benign until it progresses to NASH, which is characterised by hepatic injury, inflammation, oxidative stress and fibrosis. Hepatic fibrosis is a risk factor for cirrhosis and primary hepatocellular carcinoma. Our studies have focused on the impact of diet on the onset and progression of NASH. We developed a mouse model of NASH by feeding Ldlr-/- mice a western diet (WD), a diet moderately high in saturated and trans-fat, sucrose and cholesterol. The WD induced a NASH phenotype in Ldlr-/- mice that recapitulates many of the clinical features of human NASH. We also assessed the capacity of the dietary n-3 PUFA, i.e. EPA (20 : 5,n-3) and DHA (22 : 6,n-3), to prevent WD-induced NASH in Ldlr-/- mice. Histologic, transcriptomic, lipidomic and metabolomic analyses established that DHA was equal or superior to EPA at attenuating WD-induced dyslipidemia and hepatic injury, inflammation, oxidative stress and fibrosis. Dietary n-3 PUFA, however, had no significant effect on WD-induced changes in body weight, body fat or blood glucose. These studies provide a molecular and metabolic basis for understanding the strengths and weaknesses of using dietary n-3 PUFA to prevent NASH in human subjects.

Indexed as

FibrosisInflammationMetS metabolic syndromen-3 PUFANAFLD non-alcoholic fatty liver diseaseNASH non-alcoholic steatohepatitisNon-alcoholic steatohepatitisNOX NADPH oxidaseOxidative stressTLR Toll-like receptorWD western diet

Identifiers

PMID26282529
PMCPMC4720541
OpenAlexW2111115786

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.