Evidence mapPaperPMID 41107482Full record

ReviewNature metabolism2025

Human genetics of steatotic liver disease: insights into insulin resistance and lipid metabolism.

Rosellina M Mancina, Luca Valenti, Stefano Romeo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
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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.

Rosellina M MancinaDepartment of Life Science, Health, and Health Professions, Link Campus University, Rome, Italy. r.mancina@unilink.it.ORCID http://orcid.org/0000-0002-1126-3071
Luca ValentiDepartment of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy. luca.valenti@unimi.it.ORCID http://orcid.org/0000-0001-8909-0345
Stefano RomeoDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden. stefano.romeo@ki.se.ORCID http://orcid.org/0000-0001-9168-4898

Funding

Cancerfonden (Swedish Cancer Society) 22 2270 PjVetenskapsrådet (Swedish Research Council) 2023-02079
6 · The paper itself

Abstract

Metabolic-dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty liver disease or NAFLD) is a prevalent and heterogeneous condition affecting nearly 30% of the global population. MASLD is defined as excessive hepatic lipid accumulation with at least one feature of insulin resistance, with potential progression to metabolic dysfunction-associated steatohepatitis, cirrhosis and hepatocellular carcinoma. The disease often coexists with insulin resistance and cardiovascular and chronic kidney diseases. Human genetics has shed light on MASLD predisposition and its causal association with type 2 diabetes and insulin resistance, enabling the field to progress towards precision-medicine therapeutics. Convergent selection of somatic mutations in genes involved in glucose and lipid metabolism in cirrhotic livers suggests adaptive responses to gluco-lipotoxicity that influence end-stage liver disease. Recently, two distinct types of MASLD, with specific clinical trajectories, were identified on the basis of partitioned polygenic risk scores. Future studies are needed to integrate this knowledge, enabling earlier detection, risk stratification and targeted therapies.

Indexed as

Fatty LiverGenetic Predisposition to DiseaseInsulin ResistanceLipid MetabolismGenetic Risk ScoreGenetic VariationGlucoseHumansLiver CirrhosisMutationPrevalenceGlucose

Identifiers

What Socratic 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 Socratic graph.