Genetic variation in transmembrane 6 superfamily member 2 and the risk of nonalcoholic fatty liver disease and histological disease severity

We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically p...

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Vydané v:	Hepatology (Baltimore, Md.) Ročník 61; číslo 2; s. 515 - 525
Hlavní autori:	Sookoian, Silvia, Castaño, Gustavo O., Scian, Romina, Mallardi, Pablo, Fernández Gianotti, Tomas, Burgueño, Adriana L., San Martino, Julio, Pirola, Carlos J.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Wolters Kluwer Health, Inc 01.02.2015
Predmet:	Adult Aged Alleles Cardiovascular Diseases - genetics Case-Control Studies Confidence intervals Disease Progression Female Fibrosis Genetic Predisposition to Disease Genetic Variation Hepatology Humans Liver Liver - metabolism Liver - pathology Liver diseases Male Medical research Membrane Proteins - genetics Middle Aged Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - pathology Polymorphism, Single Nucleotide
ISSN:	0270-9139, 1527-3350, 1527-3350
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Abstract	We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02‐1.84); nevertheless, conditioning on patatin‐like phospholipase domain‐containing 3 (PNPLA3)‐rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P = 0.021; OR, 1.66; 95% CI: 1.08‐2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele‐specific transcript abundance. Conclusion: rs58542926 is a low‐frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology. (Hepatology 2015;61:515‐525)
AbstractList	We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02-1.84); nevertheless, conditioning on patatin-like phospholipase domain-containing 3 (PNPLA3)-rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P = 0.021; OR, 1.66; 95% CI: 1.08-2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele-specific transcript abundance.UNLABELLEDWe explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02-1.84); nevertheless, conditioning on patatin-like phospholipase domain-containing 3 (PNPLA3)-rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P = 0.021; OR, 1.66; 95% CI: 1.08-2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele-specific transcript abundance.rs58542926 is a low-frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology.CONCLUSIONrs58542926 is a low-frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology. We explored the role of transmembrane 6 superfamily member 2 ( TM6SF2 ) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver ( P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02‐1.84); nevertheless, conditioning on patatin‐like phospholipase domain‐containing 3 ( PNPLA3 )‐rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity ( P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression ( P = 0.021; OR, 1.66; 95% CI: 1.08‐2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele‐specific transcript abundance. Conclusion : rs58542926 is a low‐frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology. (H epatology 2015;61:515‐525) We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P=0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02-1.84); nevertheless, conditioning on patatin-like phospholipase domain-containing 3 (PNPLA3)-rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P=0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P=0.021; OR, 1.66; 95% CI: 1.08-2.55). A significant association was found with the histological degree of liver steatosis ([beta], 0.15; standard error: 0.06; P=0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele-specific transcript abundance. Conclusion: rs58542926 is a low-frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology. (Hepatology 2015;61:515-525) We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02‐1.84); nevertheless, conditioning on patatin‐like phospholipase domain‐containing 3 (PNPLA3)‐rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P = 0.021; OR, 1.66; 95% CI: 1.08‐2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele‐specific transcript abundance. Conclusion: rs58542926 is a low‐frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology. (Hepatology 2015;61:515‐525) We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model. A discrete trait analysis of NAFLD showed that rs58542926 was associated with a modest risk of fatty liver (P = 0.038; odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.02-1.84); nevertheless, conditioning on patatin-like phospholipase domain-containing 3 (PNPLA3)-rs738409 abolished this effect. We did not observe an interaction between rs738409 and rs58542926 variants on the risk of NAFLD. We observed a significant association of rs58542926 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not associated with levels of liver enzymes. An allelic test showed that the T (Lys167) allele was significantly associated with disease progression (P = 0.021; OR, 1.66; 95% CI: 1.08-2.55). A significant association was found with the histological degree of liver steatosis (β, 0.15; standard error: 0.06; P = 0.0299) that was independent of rs738409. Homozygous carriers of the C (Glu167) allele showed increased risk for cardiovascular disease. TM6SF2 protein expression was decreased markedly in liver of NAFLD patients, compared to controls. In addition, TM6SF2 immunoreactivity was reduced in subjects carrying at least one copy of the T allele, consistent with a difference in liver allele-specific transcript abundance. rs58542926 is a low-frequency variant with a modest effect on NAFLD, suggesting that carriers of the T allele are slightly more likely to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without. TM6SF2 appears to play a significant role in disease biology.
Author	Castaño, Gustavo O. Mallardi, Pablo Burgueño, Adriana L. San Martino, Julio Pirola, Carlos J. Sookoian, Silvia Scian, Romina Fernández Gianotti, Tomas
Author_xml	– sequence: 1 givenname: Silvia surname: Sookoian fullname: Sookoian, Silvia organization: Institute of Medical Research A Lanari‐IDIM, University of Buenos Aires–National Scientific and Technical Research Council (CONICET) – sequence: 2 givenname: Gustavo O. surname: Castaño fullname: Castaño, Gustavo O. organization: Hospital Abel Zubizarreta – sequence: 3 givenname: Romina surname: Scian fullname: Scian, Romina organization: Institute of Medical Research A Lanari‐IDIM, University of Buenos Aires–National Scientific and Technical Research Council (CONICET) – sequence: 4 givenname: Pablo surname: Mallardi fullname: Mallardi, Pablo organization: Hospital Diego Thompson – sequence: 5 givenname: Tomas surname: Fernández Gianotti fullname: Fernández Gianotti, Tomas organization: Institute of Medical Research A Lanari‐IDIM, University of Buenos Aires–National Scientific and Technical Research Council (CONICET) – sequence: 6 givenname: Adriana L. surname: Burgueño fullname: Burgueño, Adriana L. organization: Institute of Medical Research A Lanari‐IDIM, University of Buenos Aires–National Scientific and Technical Research Council (CONICET) – sequence: 7 givenname: Julio surname: San Martino fullname: San Martino, Julio organization: Hospital Diego Thompson – sequence: 8 givenname: Carlos J. surname: Pirola fullname: Pirola, Carlos J. organization: Institute of Medical Research A Lanari‐IDIM, University of Buenos Aires–National Scientific and Technical Research Council (CONICET)
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/25302781$$D View this record in MEDLINE/PubMed
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ContentType	Journal Article
Copyright	2014 by the American Association for the Study of Liver Diseases 2014 by the American Association for the Study of Liver Diseases. 2015 by the American Association for the Study of Liver Diseases
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Notes	Drs. Sookoian and Pirola share joint senior authorship. Potential conflict of interest: Nothing to report. This study was partially supported by grants PICT 2010‐0441 and PICT 2012‐0159 (Agencia Nacional de Promoción Científica y Tecnológica) and UBACYT CM04 (Universidad de Buenos Aires). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
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References	2013; 19 2014; 5 2014; 307 2013; 10 2009; 50 2006; 38 2008; 49 2011; 53 2002; 106 2005; 41 2008; 48 2014; 46 2011; 43 2012; 16 2000; 155 2014 2008; 83 2008; 40 2014; 95 2014; 111 2014; 61 1996; 43 2014; 12 2011; 7 (hep27556-bib-0017-20241017) 2014 (hep27556-bib-0016-20241017) 1996; 43 (hep27556-bib-0003-20241017) 2008; 40 (hep27556-bib-0027-20241017) 2011; 7 (hep27556-bib-0006-20241017) 2014; 5 (hep27556-bib-0004-20241017) 2011; 53 (hep27556-bib-0025-20241017) 2014 (hep27556-bib-0024-20241017) 2014; 111 (hep27556-bib-0001-20241017) 2013; 10 (hep27556-bib-0007-20241017) 2014; 61 (hep27556-bib-0010-20241017) 2005; 41 (hep27556-bib-0021-20241017) 2014; 12 (hep27556-bib-0013-20241017) 2014; 46 (hep27556-bib-0023-20241017) 2008; 83 (hep27556-bib-0012-20241017) 2000; 155 (hep27556-bib-0015-20241017) 2014; 95 (hep27556-bib-0009-20241017) 2002; 106 (hep27556-bib-0002-20241017) 2012; 16 (hep27556-bib-0008-20241017) 2009; 50 (hep27556-bib-0018-20241017) 2008; 48 (hep27556-bib-0019-20241017) 2008; 49 (hep27556-bib-0005-20241017) 2014; 46 (hep27556-bib-0022-20241017) 2011; 43 (hep27556-bib-0026-20241017) 2014; 307 (hep27556-bib-0014-20241017) 2006; 38 (hep27556-bib-0020-20241017) 2013; 19 (hep27556-bib-0011-20241017) 2011; 53 25502625 - Hepatology. 2015 Oct;62(4):1321-2 26206460 - Hepatology. 2016 Mar;63(3):1056-7 25502834 - Hepatology. 2015 Oct;62(4):1321
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Snippet	We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to... We explored the role of transmembrane 6 superfamily member 2 ( TM6SF2 ) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to...
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SubjectTerms	Adult Aged Alleles Cardiovascular Diseases - genetics Case-Control Studies Confidence intervals Disease Progression Female Fibrosis Genetic Predisposition to Disease Genetic Variation Hepatology Humans Liver Liver - metabolism Liver - pathology Liver diseases Male Medical research Membrane Proteins - genetics Middle Aged Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - pathology Polymorphism, Single Nucleotide
Title	Genetic variation in transmembrane 6 superfamily member 2 and the risk of nonalcoholic fatty liver disease and histological disease severity
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