Evidence map›Paper›PMID 19859993›Full record

ReviewWorld journal of gastroenterology2009

Steatosis and insulin resistance in hepatitis C: a way out for the virus?

José A Del Campo, Manuel Romero-Gómez

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Association between insulin resistance and sustained virologic response in hepatitis C treatment, genotypes 1 versus 2 and 3: systematic literature review and meta-analysis.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Review
  7. Increased Insulin Resistance in Hepatitis-C Infection-Association with Altered Hepatic Function Testing.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Hepatic steatosis in HCV-infected persons in the direct-acting antiviral era.Tropical diseases, travel medicine and vaccines · 2016
    Review
  14. Review
  15. Liver steatosis in hepatitis C patients.World journal of hepatology · 2015
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

2 authors at 2 institutions in 3 countries.

José A Del CampoUnit for The Clinical Management of Digestive Diseases and CIBERehd, Hospital Universitario de Valme, Ctra de Cadiz s/n, Sevilla 41014, Spain.
Manuel Romero-Gómez
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESHospital Universitario de Valme · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. The pathogenesis of steatosis is due to both viral and host factors. Viral steatosis is mostly reported in patients with genotype 3a, whereas metabolic steatosis is often associated with genotype 1 and metabolic syndrome. Several molecular mechanisms responsible for steatosis have been associated with the HCV core protein, which is able to induce gene expression and activity of sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor gamma (PPARgamma), increasing the transcription of genes involved in hepatic fatty acid synthesis. Steatosis has been also implicated in viral replication. In infected cells, HCV core protein is targeted to lipid droplets which serve as intracellular storage organelles. These studies have shown that lipid droplets are essential for virus assembly. Thus, HCV promotes steatosis as an efficient mechanism for stable viral replication. Chronic HCV infection can also induce insulin resistance. In patients with HCV, insulin resistance is more strongly associated with viral load than visceral obesity. HCV seems to lead to insulin resistance through interference of intracellular insulin signalling by HCV proteins, mainly, the serine phosphorylation of insulin receptor-1 (IRS-1) and impairment of the downstream Akt signalling pathway. The HCV core protein interferes with in vitro insulin signalling by genotype-specific mechanisms, where the role of suppressor of cytokine signal 7 (SOCS-7) in genotype 3a and mammalian target of rapamycin (mTOR) in genotype 1 in IRS-1 downregulation play key roles. Steatosis and insulin resistance have been associated with fibrosis progression and a reduced rate of sustained response to peginterferon plus ribavirin.

Indexed as

Insulin ResistanceDisease ProgressionFatty LiverFibrosisGenotypeHepatitis CHumansLipidsMetabolic SyndromeNuclear ProteinsPPAR gammaProtein KinasesSterol Regulatory Element Binding Protein 1Suppressor of Cytokine Signaling ProteinsTOR Serine-Threonine KinasesLipidsMTOR protein, humanNuclear ProteinsPPAR gammaProtein KinasesSOCS7 protein, humanSREBF1 protein, humanSterol Regulatory Element Binding Protein 1Suppressor of Cytokine Signaling ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID19859993
PMCPMC2768879
OpenAlexW1903688346

What OpenQuestion holds

Textmetadata
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.