Evidence map›Paper›PMID 24366230›Full record

ReviewCurrent opinion in lipidology2014

Nutrition, nonalcoholic fatty liver disease and the microbiome: recent progress in the field.

Miriam B Vos

Abstract readReview
In one paragraph

Review in Current opinion in lipidology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Trial
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  9. miR-149 controls non-alcoholic fatty liver by targeting FGF-21.Journal of cellular and molecular medicine · 2016
    Article
  10. Review
  11. Article
  12. Article
  13. Observational
  14. Review
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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

1 author.

Miriam B VosaEmory University bChildren's Healthcare of Atlanta, Atlanta, Georgia, USA.

Funding

Dietary Fructose and Redox Effects in Pediatric Nonalcoholic Fatty Liver DiseaseK23DK080953 · NIDDK · EMORY UNIVERSITY · PI VOS, MIRIAM B. · 2008 to 2012
$871k
NIDDK NIH HHS K23 DK080953
6 · The paper itself

Abstract

purpose of reviewNonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide and it has overlapping pathogenesis with diabetes and cardiovascular disease. Reviewed here are recent advances in understanding the contribution of diet and selected nutrients to NAFLD. RECENT

findingsTo understand the effect of diet, the microbiome must be considered because it is the interface of diet and the liver. Early studies suggest that the characteristic of the microbiota is altered in NAFLD. Fructose is a lipogenic carbohydrate that contributes to insulin resistance, hypertriglyceridemia and appears to be associated with the severity of NAFLD. Fructose absorption and malabsorption may alter the microbiota and could be mediating effects on the liver. Lipids also have potent microbiome interactions and could contribute to the benefit of diets emphasizing lipid changes. Several new studies demonstrate that the Mediterranean diet and 'lifestyle change' are effective in modestly improving NAFLD. A new study of 'lifestyle' in children showed simultaneous improvement in cardiovascular disease risk measurements and hepatic steatosis. SUMMARY: Current data supports limiting sugar in the diet and 'lifestyle change' as a first-line treatment for NAFLD; however, the benefits from these appear to be modest. The effects of diet on the liver are mediated through the microbiome and expansion of research in this area is needed.

Indexed as

DietMicrobiotaAnimalsFatty LiverHumansLiverNon-alcoholic Fatty Liver Disease

Identifiers

PMID24366230
PMCPMC3947892

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.