Genome‐wide association of individual vulnerability with alcohol‐associated liver disease: A Korean genome and epidemiology study

Kim, Kwangyoon; Kim, Jung Oh; Kim, Young-Sang; Choi, Ja-Eun; Park, Jaemin; Han, Kunhee; Park, Da-Hyun; Park, Yon Chul; Kim, Bom Taeck; Hong, Kyung‐Won

doi:10.1002/hep.32115

Cited by 10 publications

(6 citation statements)

References 35 publications

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“…Another recent study found three loci, ZNF827, GGT1, and HNF1A, to be significantly associated with ALD risk [144]. Other GWASs for ALD revealed candidate genes such as GABRB1, DRD4 and TH, PECR, PDLIM5, METAP, ADH1C, etc.…”

Section: Gwas Loci For Predisposition and Susceptibility Of Aldmentioning

confidence: 98%

Microbiome and Genetic Factors in the Pathogenesis of Liver Diseases

Miteva,

Peshevska-Sekulovska,

Snegarova

et al. 2023

Gastroenterology Insights

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Our genetic background has not changed over the past century, but chronic diseases are on the rise globally. In addition to the genetic component, among the critical factors for many diseases are inhabitants of our intestines (gut microbiota) as a crucial environmental factor. Dysbiosis has been described in liver diseases with different etiologies like non-alcoholic fatty liver disease (NAFLD), alcohol-related liver disease (ALD), viral hepatitis, autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), primary biliary cholangitis (PBC), cirrhosis, hepatocellular carcinoma (HCC). On the other hand, new technologies have increased our understanding of liver disease genetics and treatment options. Genome-wide association studies (GWAS) identify unknown genetic risk factors, positional cloning of unknown genes associated with different diseases, gene tests for single nucleotide variations (SNVs), and next-generation sequencing (NGS) of selected genes or the complete genome. NGS also allowed studying the microbiome and its role in various liver diseases has begun. These genes have proven their effect on microbiome composition in host genome–microbiome association studies. We focus on altering the intestinal microbiota, and supplementing some bacterial metabolites could be considered a potential therapeutic strategy. The literature data promote probiotics/synbiotics role in reducing proinflammatory cytokines such as TNF-α and the interleukins (IL-1, IL-6, IL-8), therefore improving transaminase levels, hepatic steatosis, and NAFLD activity score. However, even though microbial therapy appears to be risk-free, evaluating side effects related to probiotics or synbiotics is imperative. In addition, safety profiles for long-term usage should be researched. Thus, this review focuses on the human microbiome and liver diseases, recent GWASs on liver disease, the gut-liver axis, and the associations with the microbiome and microbiome during/after liver disease therapy.

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Section: Gwas Loci For Predisposition and Susceptibility Of Aldmentioning

confidence: 98%

Microbiome and Genetic Factors in the Pathogenesis of Liver Diseases

Miteva,

Peshevska-Sekulovska,

Snegarova

et al. 2023

Gastroenterology Insights

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“…Of note, this mechanism drives the full spectrum of fatty liver diseases, ranging from fatty liver to steatohepatitis, progressive fibrosis, cirrhosis, and HCC. [5] In this issue of Hepatology, Kim et al [6] used the KoGES (Korean Genome and Epidemiology Study) Health Examination cohort, comprising 40-to 79-year-old Korean persons from an urban area who were recruited from a national health examinee registry and genotyped by the National Biobank of Korea. [7] Based on questionnaires of 21,919 participants, they identified 782 (4.1%), 1,379 (9.5%), and 1,185 (34.5%) patients who presented with gamma-glutamyl transferase (GGT)/alanine aminotransferase >2.5 or aspartate aminotransferase/ALT > 3.0 (used as indicators of AALD) without an overt drinking history or with a history of consuming less or more than 140 g (women) and 210 g (men) of alcohol per week, respectively.…”

Section: Vulnerability To Alcohol-associated Liver Disease: a Tale Of...mentioning

confidence: 99%

“…The study by Kim et al [ 6 ] highlights that genetic susceptibility to AALD is multifactorial and suggests that genetic vulnerability is modulated by the quantity of alcohol consumed. The observations are consistent with meta‐analyses [ 8 ] reporting that alcohol consumption amplifies the genetic risk driven by PNPLA3.…”

mentioning

confidence: 99%

Vulnerability to alcohol‐associated liver disease: A tale of two systems

Karataylı

Lammert

2022

Hepatology

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“…A GWAS was carried out in the Korean Genome and Epidemiology Study Health Examination cohort data to assess the risk of developing ALD in nondrinkers, light drinkers, and heavy drinkers. The study r e p o r te d a n a s s o c i a t i o n of lo c i , n a m e l y ga m m aglutamyltransferase 1 (GGT1; rs2006227), zinc protein finger 827 (ZNF827; rs1183910), and HNF1 homeobox A (HNF1A; rs1183910) with ALD risk, in addition to 5 variants on Chromosome 11 that showed protective effects against ALD (35).…”

Section: Patatin-like Phospholipase Domaincontaining Proteinmentioning

confidence: 99%

An update on the genetics of alcoholic liver disease

Vishnubhotla¹,

Kulkarni²,

Sharma³

et al. 2022

Front. Gastroenterol.

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Worldwide, an estimated 2 billion individuals consume alcohol, which contributes to short-term or long-term consequences on health and social life. Alcohol is the cause of approximately 1.8 million deaths per year, representing 3.2% of all deaths worldwide. Of the 2 billion individuals who consume alcohol, more than 75 million are diagnosed with alcohol-use disorder (AUD) and are at an enhanced risk of developing alcoholic liver disease (ALD). However, not all individuals who consume alcohol develop liver disease suggesting the intricate interactions of host genetics with the environment in the precipitation of the phenotype. With advances in genomic technologies, it is now possible to sequence clinically relevant genomic loci associated with a phenotype with precision and faster turnaround times. Genomic data in the form of variants may be used to predict susceptibility to a phenotype in an unaffected individual or may assist the clinician in predicting the outcomes after the onset of the disease. Both of these are crucial as the former would aid in reducing the future burden of the disease, and the latter would help identify and treat individuals at risk of severe liver disease. In the current review, we summarize the pathogenic mechanisms of ALD and discuss the variants identified to date that may aid in predicting alcohol dependence and the development of cirrhosis in individuals with AUD.

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Genome‐wide association of individual vulnerability with alcohol‐associated liver disease: A Korean genome and epidemiology study

Abstract: This study was conducted with bioresources provided by the National Biobank of Korea, the Centers for Disease Control and Prevention, Republic of Korea (2019-059). The work was funded by the Ministry of Trade, Industry and Energy of Korea (20002781).

Cited by 10 publications

References 35 publications

Microbiome and Genetic Factors in the Pathogenesis of Liver Diseases

Microbiome and Genetic Factors in the Pathogenesis of Liver Diseases

Vulnerability to alcohol‐associated liver disease: A tale of two systems

An update on the genetics of alcoholic liver disease

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