Shared genetic effects between hepatic steatosis and fibrosis: A prospective twin study
Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study e...
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| Published in | Hepatology (Baltimore, Md.) Vol. 64; no. 5; pp. 1547 - 1558 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wolters Kluwer Health, Inc
01.11.2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0270-9139 1527-3350 1527-3350 |
| DOI | 10.1002/hep.28674 |
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| Abstract | Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross‐sectional analysis of a prospective cohort of well‐characterized, community‐dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging‐proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual‐specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m2, respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging‐proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716‐1, P < 0.0001). Conclusions: Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547‐1558) |
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| AbstractList | Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross‐sectional analysis of a prospective cohort of well‐characterized, community‐dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging‐proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual‐specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m
2
, respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging‐proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716‐1,
P
< 0.0001).
Conclusions
: Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (H
epatology
2016;64:1547‐1558) Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross‐sectional analysis of a prospective cohort of well‐characterized, community‐dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging‐proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual‐specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m2, respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging‐proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high‐density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716‐1, P < 0.0001). Conclusions: Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547‐1558) Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross-sectional analysis of a prospective cohort of well-characterized, community-dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual-specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m2 , respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging-proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716-1, P < 0.0001).Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross-sectional analysis of a prospective cohort of well-characterized, community-dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual-specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m2 , respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging-proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716-1, P < 0.0001).Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547-1558).CONCLUSIONSGenes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547-1558). Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross-sectional analysis of a prospective cohort of well-characterized, community-dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual-specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean ( plus or minus standard deviation) age and body mass index were 47.1 ( plus or minus 21.9) years and 26.2 ( plus or minus 5.8) kg/m super(2), respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging-proton density fat fraction greater than or equal to 5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography greater than or equal to 3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716-1, P < 0.0001). Conclusions: Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016; 64:1547-1558) Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown. This study examined the shared gene effects between hepatic steatosis and fibrosis and their associations with metabolic risk factors. This was a cross-sectional analysis of a prospective cohort of well-characterized, community-dwelling twins (45 monozygotic, 20 dizygotic twin pairs, 130 total subjects) from southern California. Hepatic steatosis was assessed with magnetic resonance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography. A standard bivariate twin additive genetics and unique environment effects model was used to estimate the proportion of phenotypic variance between two phenotypes accounted for by additive genetic effects and individual-specific environmental effects. Genetic correlations estimated from this model represent the degree to which the genetic determinants of two phenotypes overlap. Mean (± standard deviation) age and body mass index were 47.1 (±21.9) years and 26.2 (±5.8) kg/m , respectively. Among the cohort, 20% (26/130) had hepatic steatosis (magnetic resonance imaging-proton density fat fraction ≥5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography ≥3 kPa). Blood pressure (systolic and diastolic), triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic steatosis. Triglycerides, glucose, homeostatic model assessment of insulin resistance, insulin, hemoglobin A1c, and low high-density lipoprotein had significant shared gene effects with hepatic fibrosis. Hepatic steatosis and fibrosis had a highly significant shared gene effect of 0.756 (95% confidence interval 0.716-1, P < 0.0001). Genes involved with steatosis pathogenesis may also be involved with fibrosis pathogenesis. (Hepatology 2016;64:1547-1558). |
| Author | Cui, Jeffrey Hooker, Jonathan for the Genetics of NAFLD in Twins Consortium Bhatt, Archana Schork, Nicholas Loomba, Rohit Shaffer, Katherine Brenner, David A. Lo, Min‐Tzu Long, Michelle T. Nelson, Karen E. Sirlin, Claude B. Bettencourt, Ricki Chen, Chi‐Hua Gonzalez, Monica P. |
| AuthorAffiliation | 1 NAFLD Research Center, Department of Medicine, University of California at San Diego, La Jolla, CA, USA 7 J Craig Venter Institute, La Jolla, CA, USA 3 Human Biology, J Craig Venter Institute, La Jolla, CA, USA 8 Division of Gastroenterology, Department of Medicine, Boston University School of Medicine, Boston, MA 2 Department of Radiology, University of California at San Diego, La Jolla, CA, USA 5 Liver Imaging Group, Department of Radiology, University of California at San Diego, La Jolla, CA 4 Division of Epidemiology, Department of Family and Preventive Medicine, University of California at San Diego, La Jolla, CA 6 Division of Gastroenterology, Department of Medicine, University of California at San Diego, La Jolla, CA 9 Genetics of NAFLD in Twins Consortium |
| AuthorAffiliation_xml | – name: 4 Division of Epidemiology, Department of Family and Preventive Medicine, University of California at San Diego, La Jolla, CA – name: 6 Division of Gastroenterology, Department of Medicine, University of California at San Diego, La Jolla, CA – name: 9 Genetics of NAFLD in Twins Consortium – name: 3 Human Biology, J Craig Venter Institute, La Jolla, CA, USA – name: 2 Department of Radiology, University of California at San Diego, La Jolla, CA, USA – name: 1 NAFLD Research Center, Department of Medicine, University of California at San Diego, La Jolla, CA, USA – name: 5 Liver Imaging Group, Department of Radiology, University of California at San Diego, La Jolla, CA – name: 7 J Craig Venter Institute, La Jolla, CA, USA – name: 8 Division of Gastroenterology, Department of Medicine, Boston University School of Medicine, Boston, MA |
| Author_xml | – sequence: 1 givenname: Jeffrey surname: Cui fullname: Cui, Jeffrey organization: University of California at San Diego – sequence: 2 givenname: Chi‐Hua surname: Chen fullname: Chen, Chi‐Hua organization: University of California at San Diego – sequence: 3 givenname: Min‐Tzu surname: Lo fullname: Lo, Min‐Tzu organization: University of California at San Diego – sequence: 4 givenname: Nicholas surname: Schork fullname: Schork, Nicholas organization: J. Craig Venter Institute – sequence: 5 givenname: Ricki surname: Bettencourt fullname: Bettencourt, Ricki organization: University of California at San Diego – sequence: 6 givenname: Monica P. surname: Gonzalez fullname: Gonzalez, Monica P. organization: University of California at San Diego – sequence: 7 givenname: Archana surname: Bhatt fullname: Bhatt, Archana organization: University of California at San Diego – sequence: 8 givenname: Jonathan surname: Hooker fullname: Hooker, Jonathan organization: University of California at San Diego – sequence: 9 givenname: Katherine surname: Shaffer fullname: Shaffer, Katherine organization: University of California at San Diego – sequence: 10 givenname: Karen E. surname: Nelson fullname: Nelson, Karen E. organization: J. Craig Venter Institute – sequence: 11 givenname: Michelle T. surname: Long fullname: Long, Michelle T. organization: Boston University School of Medicine – sequence: 12 givenname: David A. surname: Brenner fullname: Brenner, David A. organization: University of California at San Diego – sequence: 13 givenname: Claude B. surname: Sirlin fullname: Sirlin, Claude B. organization: University of California at San Diego – sequence: 14 givenname: Rohit surname: Loomba fullname: Loomba, Rohit email: roloomba@ucsd.edu organization: University of California at San Diego – sequence: 15 surname: for the Genetics of NAFLD in Twins Consortium fullname: for the Genetics of NAFLD in Twins Consortium |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27315352$$D View this record in MEDLINE/PubMed |
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| Copyright | 2016 by the American Association for the Study of Liver Diseases 2016 by the American Association for the Study of Liver Diseases. |
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| Notes | See Editorial on Page 1417 Potential conflict of interest: Dr. Schork consults and owns stock in Human Longevity. He is employed and owns stock in MYI and CEGC. Dr. Sirlin consults for Fibrogen, Tobira, and Virtualscopic. Supported in part by the American Gastroenterological Association Foundation‐Sucampo‐ASP Designated Research Award in Geriatric Gastroenterology (to R.L.) and a T. Franklin Williams Scholarship Award (to R.L.) and by Atlantic Philanthropies Inc., the John A. Hartford Foundation, OM, the Association of Specialty Professors, and the American Gastroenterological Association (grant K23‐DK090303). Research reported in this publication was supported by the National Institute of Environmental Health Sciences of the National Institutes of Health under Award Number P42ES010337. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| References | 2015; 35 2012; 142 2004; 40 2015; 149 2004; 7 2014; 46 2013; 267 2010; 362 2011; 34 1992 2012; 36 2012; 56 2014; 60 2009; 136 2011; 7 2009; 29 2006; 355 2014; 5 2013; 58 2006; 45 2013; 10 2006; 44 2010; 139 2015; 61 2010; 28 2015; 41 2006; 47 2016; 63 2002; 347 1999; 30 2015 2008; 135 2011; 140 2008; 40 2010; 52 (hep28674-bib-0043-20241017) 2015; 61 (hep28674-bib-0040-20241017) 2010; 362 (hep28674-bib-0016-20241017) 2015; 149 (hep28674-bib-0038-20241017) 2006; 355 (hep28674-bib-0005-20241017) 2015; 149 (hep28674-bib-0014-20241017) 2015; 35 (hep28674-bib-0006-20241017) 2004; 40 (hep28674-bib-0027-20241017) 2011; 34 (hep28674-bib-0003-20241017) 2006; 44 (hep28674-bib-0018-20241017) 2006; 45 (hep28674-bib-0025-20241017) 2013; 58 (hep28674-bib-0026-20241017) 2013; 58 (hep28674-bib-0039-20241017) 2008; 135 (hep28674-bib-0041-20241017) 2010; 52 (hep28674-bib-0004-20241017) 2012; 56 (hep28674-bib-0031-20241017) 2014; 60 (hep28674-bib-0024-20241017) 2002; 347 (hep28674-bib-0028-20241017) 2010; 28 (hep28674-bib-0010-20241017) 2008; 40 (hep28674-bib-0022-20241017) 2012; 56 (hep28674-bib-0023-20241017) 2015; 61 (hep28674-bib-0029-20241017) 2012; 36 (hep28674-bib-0042-20241017) 2014; 5 (hep28674-bib-0001-20241017) 2012; 142 (hep28674-bib-0036-20241017) 2009; 136 (hep28674-bib-0009-20241017) 2015; 149 (hep28674-bib-0007-20241017) 2011; 140 (hep28674-bib-0020-20241017) 2011; 34 (hep28674-bib-0017-20241017) 2004; 40 (hep28674-bib-0002-20241017) 1999; 30 (hep28674-bib-0021-20241017) 2010; 139 (hep28674-bib-0033-20241017) 2016; 63 (hep28674-bib-0037-20241017) 2004; 7 (hep28674-bib-0030-20241017) 2013; 267 (hep28674-bib-0012-20241017) 2011; 7 (hep28674-bib-0015-20241017) 2015 (hep28674-bib-0011-20241017) 2010; 139 (hep28674-bib-0008-20241017) 2013; 10 (hep28674-bib-0035-20241017) 2006; 47 (hep28674-bib-0019-20241017) 2009; 29 (hep28674-bib-0032-20241017) 2015; 41 (hep28674-bib-0013-20241017) 2014; 46 27480050 - Hepatology. 2016 Nov;64(5):1417-1420 |
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magnetic resonance imaging and spectroscopy publication-title: J Magn Reson Imaging doi: 10.1002/jmri.22580 – volume: 267 start-page: 422 year: 2013 ident: hep28674-bib-0030-20241017 article-title: Nonalcoholic fatty liver disease: MR imaging of liver proton density fat fraction to assess hepatic steatosis publication-title: Radiology doi: 10.1148/radiol.12120896 – reference: 27480050 - Hepatology. 2016 Nov;64(5):1417-1420 |
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| SubjectTerms | Blood pressure Body mass Body mass index Cross-Sectional Studies Diseases in Twins - genetics Diseases in Twins - metabolism Dyslipidemia Environmental effects Fatty liver Fatty Liver - genetics Fatty Liver - metabolism Female Fibrosis Hemoglobin Hepatology Humans Insulin Insulin resistance Liver Cirrhosis - genetics Liver Cirrhosis - metabolism Liver diseases Magnetic resonance imaging Male Metabolism Middle Aged NMR Nuclear magnetic resonance Pathogenesis Prospective Studies Risk Factors Steatosis Triglycerides Twin studies Twins |
| Title | Shared genetic effects between hepatic steatosis and fibrosis: A prospective twin study |
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