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Abdominal fat interacts with PNPLA 3 I148M, but not with the APOC 3 variant in the pathogenesis of liver steatosis in chronic hepatitis C
Author(s) -
Zampino R.,
Coppola N.,
Cirillo G.,
Boemio A.,
Pisaturo M.,
Marrone A.,
Macera M.,
Sagnelli E.,
Perrone L.,
Adinolfi L. E.,
Miraglia del Giudice E.
Publication year - 2013
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.12053
Subject(s) - steatosis , medicine , fatty liver , genotype , gastroenterology , population , waist , hepatitis c , liver disease , steatohepatitis , biology , body mass index , genetics , disease , gene , environmental health
Summary The patatin‐like phospholipase domain‐containing 3 gene ( PNPLA 3) and the apolipoprotein C3 gene ( APOC 3) have been studied in relation to liver steatosis and liver disease outcome. The aim of this study was to evaluate the influence of PNPLA 3 p.I148M and APOC 3 rs2854116 and rs2854117 polymorphisms on the clinical and histological presentation of chronic hepatitis C in an Italian population and their relationship with viral and anthropometric parameters. Patients with hepatitis C ( n  = 166) entered the study receiving a clinical, histological, virological and biochemical evaluation. APOC 3 (rs2854116 and rs2854117) and PNPLA 3 (p.I148M) variants were genotyped. PNPLA 3 polymorphisms were associated with liver steatosis, which was significantly higher in patients with p.148I/M ( P  = 0.034) and p.148M/M ( P  = 0.004) variants than those homozygous for the PNPLA 3 wild type. Excluding patients with HCV genotype 3, the association with liver steatosis and PNPLA 3 variants was more marked (p.148I/I genotype vs p.148I/M, P  = 0.02, and vs p.148M/M, P  = 0.005). The APOC 3 polymorphism was not associated with any of the evaluated parameters. Among the interacting factors, BMI and waist circumference correlated with liver steatosis ( P  = 0.008 and 0.004, respectively). Relationship between waist circumference and liver steatosis was analysed for the different PNPLA 3 genotypes. Homozygous 148M patients showed a stronger correlation between waist circumference and steatosis than those carrying the other genotypes ( P  = 0.0047). In our hepatitis C‐infected population, the PNPLA 3 polymorphism influenced the development of liver steatosis, but not fibrosis progression. APOC 3 polymorphisms had no effect on the development of steatosis and no influence on the PNPLA 3 polymorphism. The amount of abdominal fat can increase the association of PNPLA 3 p.I148M with liver steatosis.

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