The MBOAT7-TMC4 Variant rs641738 Increases Risk of Nonalcoholic Fatty Liver Disease in Individuals of European Descent
Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase...
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| Published in | Gastroenterology (New York, N.Y. 1943) Vol. 150; no. 5; pp. 1219 - 1230.e6 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.05.2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0016-5085 1528-0012 1528-0012 |
| DOI | 10.1053/j.gastro.2016.01.032 |
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| Abstract | Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7−TMC4 is a susceptibility locus for the development and progression of NAFLD.
We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity.
The genotype rs641738 at the MBOAT7−TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7, but not TMC4, was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function.
We provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling. |
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| AbstractList | Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7−TMC4 is a susceptibility locus for the development and progression of NAFLD.
We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity.
The genotype rs641738 at the MBOAT7−TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7, but not TMC4, was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function.
We provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling. Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7-TMC4 is a susceptibility locus for the development and progression of NAFLD. We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity. The genotype rs641738 at the MBOAT7-TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7, but not TMC4, was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function. We provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling. Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7-TMC4 is a susceptibility locus for the development and progression of NAFLD.BACKGROUND & AIMSNonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7-TMC4 is a susceptibility locus for the development and progression of NAFLD.We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity.METHODSWe genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity.The genotype rs641738 at the MBOAT7-TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7, but not TMC4, was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function.RESULTSThe genotype rs641738 at the MBOAT7-TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7, but not TMC4, was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function.We provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling.CONCLUSIONSWe provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling. Background & Aims Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene ( MBOAT7 , also called LPIAT1 ) and transmembrane channel-like 4 gene ( TMC4 ) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7−TMC4 is a susceptibility locus for the development and progression of NAFLD. Methods We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic population-based probability sample of Dallas County residents) and 1149 European individuals from the Liver Biopsy Cross-Sectional Cohort. Clinical and anthropometric data were collected, and biochemical and lipidomics were measured in plasma samples from participants. A total of 2736 participants from the Dallas Heart Study also underwent proton magnetic resonance spectroscopy to measure hepatic triglyceride content. In the Liver Biopsy Cross-Sectional Cohort, a total of 1149 individuals underwent liver biopsy to diagnose liver disease and disease severity. Results The genotype rs641738 at the MBOAT7−TMC4 locus associated with increased hepatic fat content in the 2 cohorts, and with more severe liver damage and increased risk of fibrosis compared with subjects without the variant. MBOAT7 , but not TMC4 , was found to be highly expressed in the liver. The MBOAT7 rs641738 T allele was associated with lower protein expression in the liver and changes in plasma phosphatidylinositol species consistent with decreased MBOAT7 function. Conclusions We provide evidence for an association between the MBOAT7 rs641738 variant and the development and severity of NAFLD in individuals of European descent. This association seems to be mediated by changes in the hepatic phosphatidylinositol acyl-chain remodeling. Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7-TMC4 is a susceptibility locus for the development and progression of NAFLD. |
| Author | Käkelä, Pirjo Pujia, Arturo Pipitone, Rosaria Maria Montalcini, Tiziana Kärjä, Vesa Männistö, Ville Reilly, Dermot F. Pingitore, Piero Meroni, Marica Nobili, Valerio Hindy, George Pihlajamäki, Jussi Borén, Jan Dongiovanni, Paola Petta, Salvatore Mancina, Rosellina Margherita Castro-Perez, Jose Kozlitina, Julia Rametta, Raffaela Motta, Benedetta Maria Spagnuolo, Rocco Craxì, Antonio Valenti, Luca Wiklund, Olov Fargion, Silvia Romeo, Stefano |
| AuthorAffiliation | 17 Waters Corporation, Milford, Massachusetts, USA 15 Merck Research Laboratories, Genetics and Pharmacogenomics, Boston, Massachusetts, USA 9 Hepatometabolic Unit, Bambin Gesù Hospital, Rome, Italy 2 Internal Medicine, Fondazione IRCCS Ca’ Granda Ospedale Policlinico Milano, Milan, Italy 14 Department of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland 11 Department of Pathology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland 10 Department of Surgery, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland 3 Department of Gastroenterology, Università di Palermo, Palermo, Italy 12 Department of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland 16 Merck Research Laboratories, Diabetes Department, Kenilworth, New Jersey, USA 1 Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden 8 Division of Gastroenterology, Fondazione Tommaso Campanella, Univer |
| AuthorAffiliation_xml | – name: 6 Cardiology Department, Sahlgrenska University Hospital, Gothenburg, Sweden – name: 10 Department of Surgery, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland – name: 7 Diabetes and Cardiovascular Disease-Genetic Epidemiology, Lund, Sweden – name: 15 Merck Research Laboratories, Genetics and Pharmacogenomics, Boston, Massachusetts, USA – name: 17 Waters Corporation, Milford, Massachusetts, USA – name: 12 Department of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland – name: 9 Hepatometabolic Unit, Bambin Gesù Hospital, Rome, Italy – name: 2 Internal Medicine, Fondazione IRCCS Ca’ Granda Ospedale Policlinico Milano, Milan, Italy – name: 4 Department of Pathophysiology and Transplantation Università degli Studi di Milano, Milan, Italy – name: 16 Merck Research Laboratories, Diabetes Department, Kenilworth, New Jersey, USA – name: 18 McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA – name: 3 Department of Gastroenterology, Università di Palermo, Palermo, Italy – name: 1 Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – name: 13 Clinical Nutrition and Obesity Center, Kuopio University Hospital, Kuopio, Finland – name: 14 Department of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland – name: 5 Clinical Nutrition Unit, Department of Medical and Surgical Sciences, University Magna Graecia, Catanzaro, Italy – name: 8 Division of Gastroenterology, Fondazione Tommaso Campanella, University Magna Graecia of Catanzaro, Italy – name: 11 Department of Pathology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland |
| Author_xml | – sequence: 1 givenname: Rosellina Margherita surname: Mancina fullname: Mancina, Rosellina Margherita organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – sequence: 2 givenname: Paola surname: Dongiovanni fullname: Dongiovanni, Paola organization: Internal Medicine, Fondazione IRCCS Ca’ Granda Ospedale Policlinico Milano, Milan, Italy – sequence: 3 givenname: Salvatore surname: Petta fullname: Petta, Salvatore organization: Department of Gastroenterology, Università di Palermo, Palermo, Italy – sequence: 4 givenname: Piero surname: Pingitore fullname: Pingitore, Piero organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – sequence: 5 givenname: Marica orcidid: 0000-0002-4161-4178 surname: Meroni fullname: Meroni, Marica organization: Department of Pathophysiology and Transplantationm Università degli Studi di Milano, Milan, Italy – sequence: 6 givenname: Raffaela surname: Rametta fullname: Rametta, Raffaela organization: Department of Pathophysiology and Transplantationm Università degli Studi di Milano, Milan, Italy – sequence: 7 givenname: Jan surname: Borén fullname: Borén, Jan organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – sequence: 8 givenname: Tiziana surname: Montalcini fullname: Montalcini, Tiziana organization: Clinical Nutrition Unit, Department of Medical and Surgical Sciences, University Magna Graecia, Catanzaro, Italy – sequence: 9 givenname: Arturo surname: Pujia fullname: Pujia, Arturo organization: Clinical Nutrition Unit, Department of Medical and Surgical Sciences, University Magna Graecia, Catanzaro, Italy – sequence: 10 givenname: Olov surname: Wiklund fullname: Wiklund, Olov organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – sequence: 11 givenname: George surname: Hindy fullname: Hindy, George organization: Diabetes and Cardiovascular Disease-Genetic Epidemiology, Lund, Sweden – sequence: 12 givenname: Rocco orcidid: 0000-0002-0871-4644 surname: Spagnuolo fullname: Spagnuolo, Rocco organization: Division of Gastroenterology, Fondazione Tommaso Campanella, University Magna Graecia of Catanzaro, Italy – sequence: 13 givenname: Benedetta Maria surname: Motta fullname: Motta, Benedetta Maria organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden – sequence: 14 givenname: Rosaria Maria surname: Pipitone fullname: Pipitone, Rosaria Maria organization: Department of Pathophysiology and Transplantationm Università degli Studi di Milano, Milan, Italy – sequence: 15 givenname: Antonio surname: Craxì fullname: Craxì, Antonio organization: Department of Gastroenterology, Università di Palermo, Palermo, Italy – sequence: 16 givenname: Silvia surname: Fargion fullname: Fargion, Silvia organization: Internal Medicine, Fondazione IRCCS Ca’ Granda Ospedale Policlinico Milano, Milan, Italy – sequence: 17 givenname: Valerio surname: Nobili fullname: Nobili, Valerio organization: Hepatometabolic Unit, Bambin Gesù Hospital, Rome, Italy – sequence: 18 givenname: Pirjo surname: Käkelä fullname: Käkelä, Pirjo organization: Department of Surgery, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland – sequence: 19 givenname: Vesa surname: Kärjä fullname: Kärjä, Vesa organization: Department of Pathology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland – sequence: 20 givenname: Ville surname: Männistö fullname: Männistö, Ville organization: Department of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland – sequence: 21 givenname: Jussi surname: Pihlajamäki fullname: Pihlajamäki, Jussi organization: Clinical Nutrition and Obesity Center, Kuopio University Hospital, Kuopio, Finland – sequence: 22 givenname: Dermot F. surname: Reilly fullname: Reilly, Dermot F. organization: Merck Research Laboratories, Genetics and Pharmacogenomics, Boston, Massachusetts – sequence: 23 givenname: Jose surname: Castro-Perez fullname: Castro-Perez, Jose organization: Merck Research Laboratories, Diabetes Department, Kenilworth, New Jersey – sequence: 24 givenname: Julia surname: Kozlitina fullname: Kozlitina, Julia email: Julia.Kozlitina@UTSouthwestern.edu organization: McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas – sequence: 25 givenname: Luca orcidid: 0000-0001-8909-0345 surname: Valenti fullname: Valenti, Luca email: luca.valenti@unimi.it organization: Internal Medicine, Fondazione IRCCS Ca’ Granda Ospedale Policlinico Milano, Milan, Italy – sequence: 26 givenname: Stefano surname: Romeo fullname: Romeo, Stefano email: stefano.romeo@wlab.gu.se organization: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26850495$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/232892$$DView record from Swedish Publication Index |
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| Copyright | 2016 AGA Institute AGA Institute Copyright © 2016 AGA Institute. Published by Elsevier Inc. All rights reserved. |
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| CorporateAuthor | Lunds universitet Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Diabetes - Cardiovascular Disease Strategiska forskningsområden (SFO) EXODIAB: Excellence of Diabetes Research in Sweden Faculty of Medicine Strategic research areas (SRA) Diabetes - kardiovaskulär sjukdom Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Institutionen för kliniska vetenskaper, Malmö |
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| Keywords | T2DM NAFLD OR CI MBOAT7 mRNA IFG NASH ER TMC4 DHS TM6SF2 HWE PNPLA3 PI Arachidonic Acid BMI patatin-like phospholipase domain-containing 3 transmembrane 6 superfamily member 2 odds ratio nonalcoholic steatohepatitis membrane bound O-acyltransferase domain containing 7 impaired fasting glucose messenger RNA type 2 diabetes mellitus Dallas Heart Study body mass index nonalcoholic fatty liver disease phosphatidylinositol transmembrane channel-like 4 Hardy-Weinberg equilibrium confidence interval endoplasmic reticulum |
| Language | English |
| License | Copyright © 2016 AGA Institute. Published by Elsevier Inc. All rights reserved. |
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| PublicationTitle | Gastroenterology (New York, N.Y. 1943) |
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| Snippet | Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive... Background & Aims Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk... |
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| SubjectTerms | Acetyltransferases - genetics Acetyltransferases - metabolism Acyltransferases - genetics Acyltransferases - metabolism Arachidonic Acid Biopsy Cardiology and Cardiovascular Disease Case-Control Studies Clinical Medicine Cross-Sectional Studies Europe - epidemiology European Continental Ancestry Group - genetics Female Gastroenterologi och hepatologi Gastroenterology and Hepatology Genetic Predisposition to Disease Genome-Wide Association Study Humans Kardiologi och kardiovaskulära sjukdomar Klinisk medicin Liver - metabolism Liver - pathology Liver Cirrhosis - diagnosis Liver Cirrhosis - ethnology Liver Cirrhosis - genetics Liver Cirrhosis - metabolism Male Medical and Health Sciences Medicin och hälsovetenskap Membrane Proteins - genetics Membrane Proteins - metabolism NASH Non-alcoholic Fatty Liver Disease - diagnosis Non-alcoholic Fatty Liver Disease - ethnology Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - metabolism Phenotype Phosphatidylinositols - metabolism PNPLA3 Polymorphism, Genetic Proton Magnetic Resonance Spectroscopy Risk Factors Severity of Illness Index Texas - epidemiology TM6SF2 Triglycerides - metabolism |
| Title | The MBOAT7-TMC4 Variant rs641738 Increases Risk of Nonalcoholic Fatty Liver Disease in Individuals of European Descent |
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