Evidence map›Paper›PMID 25045276›Full record

ReviewClinical and experimental gastroenterology2014

Molecular pathways in non-alcoholic fatty liver disease.

Alba Berlanga, Esther Guiu-Jurado, José Antonio Porras, Teresa Auguet

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and experimental gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
27.9field-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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 384 citations in OpenAlex.

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  18. Journal of microbiology and biotechnology · 2024
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117 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

4 authors at 2 institutions in 1 country.

Alba BerlangaGroup GEMMAIR (AGAUR) and Applied Medicine Research Group, Department of Medicine and Surgery, Universitat Rovira i Virgili (URV), IISPV, Hospital Universitari Joan XXIII, Tarragona, Spain.
Esther Guiu-JuradoGroup GEMMAIR (AGAUR) and Applied Medicine Research Group, Department of Medicine and Surgery, Universitat Rovira i Virgili (URV), IISPV, Hospital Universitari Joan XXIII, Tarragona, Spain.
José Antonio PorrasGroup GEMMAIR (AGAUR) and Applied Medicine Research Group, Department of Medicine and Surgery, Universitat Rovira i Virgili (URV), IISPV, Hospital Universitari Joan XXIII, Tarragona, Spain ; Department of Internal Medicine, Hospital Universitari Joan XXIII Tarragona, Tarragona, Spain.
Teresa AuguetGroup GEMMAIR (AGAUR) and Applied Medicine Research Group, Department of Medicine and Surgery, Universitat Rovira i Virgili (URV), IISPV, Hospital Universitari Joan XXIII, Tarragona, Spain ; Department of Internal Medicine, Hospital Universitari Joan XXIII Tarragona, Tarragona, Spain.
Universidad Rovira i Virgili · ESInstitut d'Investigació Sanitària Pere Virgili · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological change characterized by the accumulation of triglycerides in hepatocytes and has frequently been associated with obesity, type 2 diabetes mellitus, hyperlipidemia, and insulin resistance. It is an increasingly recognized condition that has become the most common liver disorder in developed countries, affecting over one-third of the population and is associated with increased cardiovascular- and liver-related mortality. NAFLD is a spectrum of disorders, beginning as simple steatosis. In about 15% of all NAFLD cases, simple steatosis can evolve into non-alcoholic steatohepatitis, a medley of inflammation, hepatocellular injury, and fibrosis, often resulting in cirrhosis and even hepatocellular cancer. However, the molecular mechanism underlying NAFLD progression is not completely understood. Its pathogenesis has often been interpreted by the "double-hit" hypothesis. The primary insult or the "first hit" includes lipid accumulation in the liver, followed by a "second hit" in which proinflammatory mediators induce inflammation, hepatocellular injury, and fibrosis. Nowadays, a more complex model suggests that fatty acids (FAs) and their metabolites may be the true lipotoxic agents that contribute to NAFLD progression; a multiple parallel hits hypothesis has also been suggested. In NAFLD patients, insulin resistance leads to hepatic steatosis via multiple mechanisms. Despite the excess hepatic accumulation of FAs in NAFLD, it has been described that not only de novo FA synthesis is increased, but FAs are also taken up from the serum. Furthermore, a decrease in mitochondrial FA oxidation and secretion of very-low-density lipoproteins has been reported. This review discusses the molecular mechanisms that underlie the pathophysiological changes of hepatic lipid metabolism that contribute to NAFLD.

Indexed as

fatty acid metabolisminsulin resistancemolecular pathwaysnon-alcoholic fatty liver disease

Identifiers

PMID25045276
PMCPMC4094580
OpenAlexW1999617321

What OpenQuestion holds

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LicenceCC BY-NC
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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.