Evidence map›Paper›PMID 28878197›Full record

ReviewNutrients2017

Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease.

Kasper W Ter Horst, Mireille J Serlie

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 6 pooled it
17.0field-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

179 citing papers in PubMed, 6 syntheses or guidelines pooled it, 353 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Evaluating the cardio-protective effects ofCardiovascular endocrinology & metabolism · 2026
    Article
  15. ChREBP-β Exacerbates Renal Tubular Disorders Caused by Fructose via ATF4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

119 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Kasper W Ter HorstDepartment of Endocrinology and Metabolism, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands. k.w.terhorst@amc.nl.ORCID 0000-0002-0502-4023
Mireille J SerlieDepartment of Endocrinology and Metabolism, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands. m.j.serlie@amc.nl.
Amsterdam UMC Location University of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased fructose consumption has been suggested to contribute to non-alcoholic fatty liver disease (NAFLD), dyslipidemia, and insulin resistance, but a causal role of fructose in these metabolic diseases remains debated. Mechanistically, hepatic fructose metabolism yields precursors that can be used for gluconeogenesis and de novo lipogenesis (DNL). Fructose-derived precursors also act as nutritional regulators of the transcription factors, including ChREBP and SREBP1c, that regulate the expression of hepatic gluconeogenesis and DNL genes. In support of these mechanisms, fructose intake increases hepatic gluconeogenesis and DNL and raises plasma glucose and triglyceride levels in humans. However, epidemiological and fructose-intervention studies have had inconclusive results with respect to liver fat, and there is currently no good human evidence that fructose, when consumed in isocaloric amounts, causes more liver fat accumulation than other energy-dense nutrients. In this review, we aim to provide an overview of the seemingly contradicting literature on fructose and NAFLD. We outline fructose physiology, the mechanisms that link fructose to NAFLD, and the available evidence from human studies. From this framework, we conclude that the cellular mechanisms underlying hepatic fructose metabolism will likely reveal novel targets for the treatment of NAFLD, dyslipidemia, and hepatic insulin resistance. Finally, fructose-containing sugars are a major source of excess calories, suggesting that a reduction of their intake has potential for the prevention of NAFLD and other obesity-related diseases.

Indexed as

Energy MetabolismLipogenesisAnimalsDietary SugarsEnergy IntakeFructoseHumansLiverNon-alcoholic Fatty Liver DiseaseRisk FactorsDietary SugarsFructoseChREBPde novo lipogenesisfructosehepatic steatosisinsulin resistancelipid synthesismetabolic syndromeNAFLDobesity

Identifiers

PMID28878197
PMCPMC5622741
OpenAlexW2751789497

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.