| Autor: |
Sales RC; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. c.sales.rafael@gmail.com., Medeiros PC; Faculdade de Medicina, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21044-020, Brazil. pri.biomed3@gmail.com., Spreafico F; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. flaviasfer@gmail.com.; Laboratory of Epigenetics of Lipid Metabolism, Madrid Institute for Advanced Studies (IMDEA)-Food, CEI UAM+CSIC, 28049 Madrid, Spain. flaviasfer@gmail.com., de Velasco PC; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. patriciac.velasco@gmail.com., Gonçalves FKA; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. fernandakgst@gmail.com., Martín-Hernández R; GENYAL Platform on Nutrition and Health, Madrid Institute for Advanced Studies (IMDEA)-Food, CEI UAM+CSIC, 28049 Madrid, Spain. roberto.martin@imdea.org., Mantilla-Escalante DC; Laboratory of Epigenetics of Lipid Metabolism, Madrid Institute for Advanced Studies (IMDEA)-Food, CEI UAM+CSIC, 28049 Madrid, Spain. diana.mantilla@imdea.org., Gil-Zamorano J; Laboratory of Epigenetics of Lipid Metabolism, Madrid Institute for Advanced Studies (IMDEA)-Food, CEI UAM+CSIC, 28049 Madrid, Spain. judit.gil@imdea.org., Peres WAF; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. wilza@nutricao.ufrj.br., de Souza SAL; Faculdade de Medicina, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21044-020, Brazil. sergioalsouza@gmail.com., Dávalos A; Laboratory of Epigenetics of Lipid Metabolism, Madrid Institute for Advanced Studies (IMDEA)-Food, CEI UAM+CSIC, 28049 Madrid, Spain. alberto.davalos@imdea.org., Tavares do Carmo MG; Instituto de Nutrição Josué de Castro, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil. tcarmo@editema.com.br. |
| Abstrakt: |
Nonalcoholic fatty liver disease (NAFLD) is highly prevalent worldwide. The most severe form is nonalcoholic steatohepatitis (NASH). Among risk factors for the development of NAFLD is excessive lipid intake. Since palm (P) oil is the most consumed oil in the world, we aimed to investigate the effects of high-fat diets made with P oil, hybrid palm (HP) oil, or olive (O) oil in liver. Twenty-four male mice (C57Bl/6J) were fed a high-fat diet (41% fat) containing P, HP, or O oils for 8 weeks and compared to a control (C) group fed a chow diet. Adiposity was measured with computed tomography. Body, adipose tissue, and liver weights, as well as liver fat (Bligh⁻Dyer), blood lipid profile, glucose, and liver enzymes were measured. Liver histology (hematoxylin⁻eosin) and transcriptome (microarray-based) were performed. ANOVA tests with Newman⁻Keuls were used. Body weight was increased in the P group ( p < 0.001) and body fat in the O group (C vs. O p ≤ 0.01, P vs. O p ≤ 0.05, HP vs. O p ≤ 0.05). All high-fat diets disturbed the blood lipid profile and glucose, with marked effects of HP on very low-density lipoprotein cholesterol (VLDL), triglycerides, and alkaline phosphatase ( p ≤ 0.001). HP had the highest liver fat (42.76 ± 1.58), followed by P (33.94 ± 1.13). O had a fat amount comparable to C (16.46 ± 0.34, 14.71 ± 0.70, respectively). P and HP oils induced hepatocyte ballooning. Transcriptome alterations of the O group were related to amino acid metabolism and fatty acid (FA) metabolism, the P group to calcium ion homeostasis, and HP oil to protein localization. Both P and HP oils induced NASH in mice via disturbed hepatocyte transcription. This raises concerns about the content of these oils in several industrialized foods. |
