Evidence map›Paper›PMID 23714158›Full record

ReviewJournal of hepatology2013

The metabolomic window into hepatobiliary disease.

Diren Beyoğlu, Jeffrey R Idle

Open access · greenAbstract readReview
In one paragraph

Review in Journal of hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
10.6field-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

111 citing papers in PubMed, 216 citations in OpenAlex.

  1. [Molecular imaging and biology · 2017
    Trial
  2. Trial
  3. Article
  4. Article
  5. Yin-Dan-Ping-Gan Capsule Mitigates CCLPharmaceuticals (Basel, Switzerland) · 2026
    Article
  6. Review
  7. Article
  8. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. A novel protein extracted fromFood science and biotechnology · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

51 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.

Diren BeyoğluHepatology Research Group, Department of Clinical Research, University of Bern, Bern, Switzerland.
Jeffrey R Idle
University of Bern · CH

Funding

Sample Engineering CoreU19AI067773 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FORNACE, ALBERT J · 2005 to 2024
$105.4M
NIAID NIH HHS U19 AI067773
6 · The paper itself

Abstract

The emergent discipline of metabolomics has attracted considerable research effort in hepatology. Here we review the metabolomic data for non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), cirrhosis, hepatocellular carcinoma (HCC), cholangiocarcinoma (CCA), alcoholic liver disease (ALD), hepatitis B and C, cholecystitis, cholestasis, liver transplantation, and acute hepatotoxicity in animal models. A metabolomic window has permitted a view into the changing biochemistry occurring in the transitional phases between a healthy liver and hepatocellular carcinoma or cholangiocarcinoma. Whether provoked by obesity and diabetes, alcohol use or oncogenic viruses, the liver develops a core metabolomic phenotype (CMP) that involves dysregulation of bile acid and phospholipid homeostasis. The CMP commences at the transition between the healthy liver (Phase 0) and NAFLD/NASH, ALD or viral hepatitis (Phase 1). This CMP is maintained in the presence or absence of cirrhosis (Phase 2) and whether or not either HCC or CCA (Phase 3) develops. Inflammatory signalling in the liver triggers the appearance of the CMP. Many other metabolomic markers distinguish between Phases 0, 1, 2 and 3. A metabolic remodelling in HCC has been described but metabolomic data from all four Phases demonstrate that the Warburg shift from mitochondrial respiration to cytosolic glycolysis foreshadows HCC and may occur as early as Phase 1. The metabolic remodelling also involves an upregulation of fatty acid β-oxidation, also beginning in Phase 1. The storage of triglycerides in fatty liver provides high energy-yielding substrates for Phases 2 and 3 of liver pathology. The metabolomic window into hepatobiliary disease sheds new light on the systems pathology of the liver.

Indexed as

AnimalsBile Duct NeoplasmsBiliary Tract DiseasesCarcinoma, HepatocellularChemical and Drug Induced Liver InjuryCholangiocarcinomaCholecystitisCholestasisDisease ProgressionFatty LiverHepatitis B, ChronicHepatitis C, ChronicHumansLiver CirrhosisLiver DiseasesLiver Diseases, AlcoholicCirrhosisCore metabolomic phenotypeHepatocellular carcinomaMetabolic remodellingMetabolomicsNAFLDNASHWarburg effect

Identifiers

PMID23714158
PMCPMC4095886
OpenAlexW2069386166

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.