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Provedor de dados:  BJMBR
País:  Brazil
Título:  MTP -493G/T gene polymorphism is associated with steatosis in hepatitis C-infected patients
Autores:  Siqueira,E.R.F.
Oliveira,C.P.M.S.
Correa-Giannella,M.L.
Stefano,J.T.
Cavaleiro,A.M.
Fortes,M.A.H.Z.
Muniz,M.T.C.
Silva,F.S.
Pereira,L.M.M.B.
Carrilho,F.J.
Data:  2012-01-01
Ano:  2012
Palavras-chave:  Hepatitis C
Steatosis
Fibrosis
Microsomal transfer protein
Resumo:  The reduction of hepatic microsomal transfer protein (MTP) activity results in fatty liver, worsening hepatic steatosis and fibrosis in chronic hepatitis C (CHC). The G allele of the MTP gene promoter, -493G/T, has been associated with lower transcriptional activity than the T allele. We investigated this association with metabolic and histological variables in patients with CHC. A total of 174 untreated patients with CHC were genotyped for MTP -493G/T by direct sequencing using PCR. All patients were negative for markers of Wilson’s disease, hemochromatosis and autoimmune diseases and had current and past daily alcohol intake lower than 100 g/week. The sample distribution was in Hardy-Weinberg equilibrium. Among subjects with genotype 1, 56.8% of the patients with fibrosis grade 3+4 presented at least one G allele versus 34.3% of the patients with fibrosis grade 1+2 (OR = 1.8; 95%CI = 1.3-2.3). Logistic regression analysis with steatosis as the dependent variable identified genotypes GG+GT as independent protective factors against steatosis (OR = 0.4, 95%CI = 0.2-0.8; P = 0.01). The results suggest that the presence of the G allele of MTP -493G/T associated with lower hepatic MTP expression protects against steatosis in our CHC patients.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2012000100012
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2011007500160
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.45 n.1 2012
Direitos:  info:eu-repo/semantics/openAccess
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