Evidence map›Paper›PMID 20207596›Full record

ReviewDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver2010

From the metabolic syndrome to NAFLD or vice versa?

Ester Vanni, Elisabetta Bugianesi, Anna Kotronen, Samuele De Minicis, Hannele Yki-Järvinen, Gianluca Svegliati-Baroni

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02964715 (The Effect of Empagliflozin on NAFLD in Asian Patients With Type 2 Diabetes), which is not on this map. Cited by 217 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed, 5 pooled it
25.6field-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.

NCT02964715 phase4unknown statusstarted 2016, after this paper: background citation

The Effect of Empagliflozin on NAFLD in Asian Patients With Type 2 Diabetes

Ran2016Enrolled25Registered outcomes17Posted comparisons0ConditionsNAFLD, Type2 DiabetesArmsempagliflozin
Open the trial in the graph
3 · Its place in the literature

Who cites it

217 citing papers in PubMed, 5 syntheses or guidelines pooled it, 489 citations in OpenAlex.

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  18. Prevalence and impact of metabolic associated fatty liver disease in non-metastatic breast cancer women at initial diagnosis: a cross-sectional study in China.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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157 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

6 authors at 3 institutions in 2 countries.

Ester VanniDivision of Gastro-Hepatology, San Giovanni Battista Hospital, University of Turin, C. so Bramante 88, 10126 Turin, Italy.
Elisabetta Bugianesi
Anna Kotronen
Samuele De Minicis
Hannele Yki-Järvinen
Gianluca Svegliati-Baroni
Marche Polytechnic University · ITUniversity of Helsinki · FIUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabolic syndrome encompasses metabolic and cardiovascular risk factors which predict diabetes and cardiovascular disease (CVD) better than any of its individual components. Nonalcoholic fatty liver disease (NAFLD) comprises a disease spectrum which includes variable degrees of simple steatosis (nonalcoholic fatty liver, NAFL), nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is the hepatic manifestation of the metabolic syndrome, with insulin resistance as the main pathogenetic mechanism. Recent data indicate that hyperinsulinemia is probably the consequence rather than cause of NAFLD and NAFLD can be considered an independent predictor of cardiovascular disease. Serum free fatty acids derived from lipolysis of visceral adipose tissue are the main source of hepatic triglycerides in NAFLD, although hepatic de novo lipogenesis and dietary fat supply contribute to the pathogenesis of NAFLD. Approximately 10-25% NAFLD patients develop NASH, the evolutive form of hepatic steatosis. Presumably in a genetically predisposed environment, this increased lipid overload overwhelms the oxidative capacity and reactive oxygen species are generated, leading to lipid peroxidation, cytokine induction, chemoattraction of inflammatory cells, hepatic stellate cell activation and finally fibrogenesis with extracellular matrix deposition. No currently available therapies for NAFLD and NASH exist. Recently nuclear receptors have emerged as key regulators of lipid and carbohydrate metabolism for which specific pharmacological ligands are available, making them attractive therapeutic targets for NAFLD and NASH.

Indexed as

Adipose TissueFatty LiverGenetic Predisposition to DiseaseHumansInsulin ResistanceMetabolic SyndromePeroxisome Proliferator-Activated ReceptorsPeroxisome Proliferator-Activated Receptors

Identifiers

PMID20207596
OpenAlexW2001940599

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.