Evidence map›Paper›PMID 26005677›Full record

ReviewHepatobiliary surgery and nutrition2015

Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction.

Metin Basaranoglu, Gokcen Basaranoglu, Elisabetta Bugianesi

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Hepatobiliary surgery and nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03783195 (Genetic-specific Effects of Fructose on Liver Lipogenesis), which is not on this map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
10.5field-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.

NCT03783195 nacompletednot on this mapstarted 2019, after this paper: background citation

Genetic-specific Effects of Fructose on Liver Lipogenesis

TypeinterventionalSponsorUniversity of North Carolina, Chapel HillRan2019 to 2023Enrolled15ConditionsNAFLDArmsSugar drink
3 · Its place in the literature

Who cites it

105 citing papers in PubMed, 174 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Fructose induces inflammatory activation in macrophages and microglia through the nutrient-sensing ghrelin receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  15. Review
  16. Review
  17. International journal of molecular sciences · 2024
    Article
  18. Article
  19. Article
  20. Review

45 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

3 authors at 1 institution in 2 countries.

Metin Basaranoglu1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, 2 Department of Anaesthesiology, Bezmialem Vakif University Faculty Hospital, Istanbul, Turkey ; 3 Division of Gastroenterology and Hepatology, Department of Medical Sciences, University of Torino, Turin, Italy.
Gokcen Basaranoglu1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, 2 Department of Anaesthesiology, Bezmialem Vakif University Faculty Hospital, Istanbul, Turkey ; 3 Division of Gastroenterology and Hepatology, Department of Medical Sciences, University of Torino, Turin, Italy.
Elisabetta Bugianesi1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, 2 Department of Anaesthesiology, Bezmialem Vakif University Faculty Hospital, Istanbul, Turkey ; 3 Division of Gastroenterology and Hepatology, Department of Medical Sciences, University of Torino, Turin, Italy.
Bezmiâlem Vakıf Üniversitesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive accumulation of triglycerides (TG) in liver, in the absence of significant alcohol consumption is nonalcoholic fatty liver disease (NAFLD). NAFLD is a significant risk factor for developing cirrhosis and an independent predictor of cardiovascular disease. High fructose corn syrup (HFCS)-containing beverages were associated with metabolic abnormalities, and contributed to the development of NAFLD in human trials. Ingested carbohydrates are a major stimulus for hepatic de novo lipogenesis (DNL) and are more likely to directly contribute to NAFLD than dietary fat. Substrates used for the synthesis of newly made fatty acids by DNL are primarily glucose, fructose, and amino acids. Epidemiological studies linked HFCS consumption to the severity of fibrosis in patients with NAFLD. New animal studies provided additional evidence on the role of carbohydrate-induced DNL and the gut microbiome in NAFLD. The excessive consumption of HFCS-55 increased endoplasmic reticulum stress, activated the stress-related kinase, caused mitochondrial dysfunction, and increased apoptotic activity in the liver. A link between dietary fructose intake, increased hepatic glucose transporter type-5 (Glut5) (fructose transporter) gene expression and hepatic lipid peroxidation, MyD88, TNF-α levels, gut-derived endotoxemia, toll-like receptor-4, and NAFLD was reported. The lipogenic and proinflammatory effects of fructose appear to be due to transient ATP depletion by its rapid phosphorylation within the cell and from its ability to raise intracellular and serum uric acid levels. However, large prospective studies that evaluated the relationship between fructose and NAFLD were not performed yet.

Indexed as

carbohydratede novo lipogenesis (DNL)high fructose corn syrup (HFCS)Nonalcoholic fatty liver disease (NAFLD)

Identifiers

PMID26005677
PMCPMC4405421
OpenAlexW1878326454

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.