ArticleScientific reports2023
Evidence for involvement of the alcohol consumption WDPCP gene in lipid metabolism, and liver cirrhosis.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
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- Unravelling genetic susceptibility and causal factors in liver health using MRI quantification of inflammation, fat and iron in the liver.Human genomics · 2026Article
- Research Trends and Hotspots in Mendelian Randomization Studies of Liver Diseases: A Bibliometric and Visualization Analysis.Hepatic medicine : evidence and research · 2026Review
- Long-read whole-genome sequencing of SHR rat substrains with distinct substance use phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Comparative Transcriptome Analysis of Hens' Livers in Conventional Cage vs. Cage-Free Egg Production Systems.Veterinary medicine international · 2025Article
- A cross-tissue transcriptome-wide association study identifies WDPCP as a potential susceptibility gene for coronary atherosclerosis.Atherosclerosis plus · 2024Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 2 countries.
Funding
Abstract
Biological pathways between alcohol consumption and alcohol liver disease (ALD) are not fully understood. We selected genes with known effect on (1) alcohol consumption, (2) liver function, and (3) gene expression. Expression of the orthologs of these genes in Caenorhabditis elegans and Drosophila melanogaster was suppressed using mutations and/or RNA interference (RNAi). In humans, association analysis, pathway analysis, and Mendelian randomization analysis were performed to identify metabolic changes due to alcohol consumption. In C. elegans, we found a reduction in locomotion rate after exposure to ethanol for RNAi knockdown of ACTR1B and MAPT. In Drosophila, we observed (1) a change in sedative effect of ethanol for RNAi knockdown of WDPCP, TENM2, GPN1, ARPC1B, and SCN8A, (2) a reduction in ethanol consumption for RNAi knockdown of TENM2, (3) a reduction in triradylglycerols (TAG) levels for RNAi knockdown of WDPCP, TENM2, and GPN1. In human, we observed (1) a link between alcohol consumption and several metabolites including TAG, (2) an enrichment of the candidate (alcohol-associated) metabolites within the linoleic acid (LNA) and alpha-linolenic acid (ALA) metabolism pathways, (3) a causal link between gene expression of WDPCP to liver fibrosis and liver cirrhosis. Our results imply that WDPCP might be involved in ALD.
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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.