Your browser doesn't support javascript.
loading
Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c.
Dossi, Camila G; Tapia, Gladys S; Espinosa, Alejandra; Videla, Luis A; D'Espessailles, Amanda.
Afiliação
  • Dossi CG; Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Tapia GS; Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Espinosa A; Department of Medical Technology, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Videla LA; Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
  • D'Espessailles A; Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile. Electronic address: adespessailles@ug.uchile.cl.
J Nutr Biochem ; 25(9): 977-84, 2014 Sep.
Article em En | MEDLINE | ID: mdl-24993917
Nonalcoholic fatty liver disease is characterized by an abnormal accumulation of triacylglycerides in the liver in absence of significant alcohol consumption. Under these conditions, it has been observed an impaired bioavailability of hepatic n-3 long-chain polyunsaturated fatty acids (LCPUFAs). The aim of this study was to test the reversion of the prosteatotic and proinflammatory effects of high-fat diet (HFD) in the mouse liver by changing to normocaloric diet and n-3 LCPUFA supplementation. Male C57BL/6J mice were given either control diet (CD) or HFD for 12 weeks. Control and HFD groups were divided into subgroups that continue with CD or subjected to CD plus n-3 LCPUFA for 8 additional weeks. After this time, blood and liver samples were taken and metabolic, morphologic, oxidative stress, inflammatory and signaling parameters were analyzed. The dietary change from HFD to a normocaloric diet with n-3 LCPUFA supplementation significantly reduced insulin resistance and liver steatosis when compared to switching HFD to normocaloric diet alone. In addition, HFD-induced increases in adiposity, adipocyte enlargement and liver oxidative stress and inflammatory cytokine expression were suppressed by n-3 LCPUFA to control values. Importantly, n-3 LCPUFA supplementation abolish HFD-induced enhancement in hepatic SREBP-1c/PPAR-α ratios, suggesting a change in the metabolic status of the liver from a lipogenic condition to one favoring fatty acid oxidation and steatosis attenuation. These findings may provide the rational basis for the use of normocaloric diets supplemented with n-3 LCPUFA in patients with liver steatosis.
Assuntos
Palavras-chave
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ácidos Graxos Ômega-3 / PPAR alfa / Proteína de Ligação a Elemento Regulador de Esterol 1 / Fígado Gorduroso / Dieta Hiperlipídica Tipo de estudo: Etiology_studies Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Chile País de publicação: Estados Unidos
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ácidos Graxos Ômega-3 / PPAR alfa / Proteína de Ligação a Elemento Regulador de Esterol 1 / Fígado Gorduroso / Dieta Hiperlipídica Tipo de estudo: Etiology_studies Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Chile País de publicação: Estados Unidos