ArticleHepatology communications2019
Insulin Resistance Exacerbates Genetic Predisposition to Nonalcoholic Fatty Liver Disease in Individuals Without Diabetes.
Article in Hepatology communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- Genetics of MASLD: a diabetes perspective.Diabetologia · 2026Review
- Genetic and genomic insights across the steatotic liver disease spectrum.Clinical and molecular hepatology · 2026Review
- Article
- PNPLA3 I148M variant links to adverse metabolic traits in MASLD during fasting and feeding.JHEP reports : innovation in hepatology · 2025Article
- Human genetics of metabolic dysfunction-associated steatotic liver disease: from variants to cause to precision treatment.The Journal of clinical investigation · 2025Review
- PNPLA3 I148M Interacts With Environmental Triggers to Cause Human Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Precision medicine and nucleotide-based therapeutics to treat steatotic liver disease.Clinical and molecular hepatology · 2025Review
- A Very Low-Carbohydrate Program in Adults With Metabolic Dysfunction-Associated Steatotic Liver Disease and Phospholipase Domain-Containing Protein 3 Risk Genotype: Pre-Post Intervention Study.JMIR formative research · 2025Article
- Therapeutic Potential ofFood science & nutrition · 2025Article
- Genetic risk accentuates dietary effects on hepatic steatosis, inflammation and fibrosis in a population-based cohort.Journal of hepatology · 2024Article
- Hepatic glucose metabolism in the steatotic liver.Nature reviews. Gastroenterology & hepatology · 2024Review
- Effect of donorEClinicalMedicine · 2024Article
- Unraveling the pathogenesis of non-alcoholic fatty liver diseases through genome-wide association studies.Journal of gastroenterology and hepatology · 2023Review
- Evaluation of Human Hepatocyte Drug Metabolism Carrying High-Risk or Protection-Associated Liver Disease Genetic Variants.International journal of molecular sciences · 2023Article
- PNPLA3 Genotype and Diabetes Identify Patients With Nonalcoholic Fatty Liver Disease at High Risk of Incident Cirrhosis.Gastroenterology · 2023Article
- Plasma Metabolite Signatures in Male Carriers of Genetic Variants Associated with Non-Alcoholic Fatty Liver Disease.Metabolites · 2023Article
- Glucokinase regulatory protein: a balancing act between glucose and lipid metabolism in NAFLD.Frontiers in endocrinology · 2023Review
- Contribution of a genetic risk score to ethnic differences in fatty liver disease.Liver international : official journal of the International Association for the Study of the Liver · 2022Article
- Influence of Type 2 Diabetes in the Association ofBiomedicines · 2022Article
- The genetic interactions between non-alcoholic fatty liver disease and cardiovascular diseases.Frontiers in genetics · 2022Review
Corrections and comments
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Authors and funding
30 authors at 9 institutions in 2 countries.
Funding
Abstract
The accumulation of excess fat in the liver (hepatic steatosis) in the absence of heavy alcohol consumption causes nonalcoholic fatty liver disease (NAFLD), which has become a global epidemic. Identifying metabolic risk factors that interact with the genetic risk of NAFLD is important for reducing disease burden. We tested whether serum glucose, insulin, insulin resistance, triglyceride (TG), low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, body mass index (BMI), and waist-to-hip ratio adjusted for BMI interact with genetic variants in or near the patatin-like phospholipase domain containing 3 (
Identifiers
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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.