Gonzalo Torres-Villalobos1, Nashla Hamdan-Pérez2, Armando R Tovar3, Guillermo Ordaz-Nava3, Braulio Martínez-Benítez4, Iván Torre-Villalvazo3, Sofía Morán-Ramos3, Andrea Díaz-Villaseñor3, Lilia G Noriega3, Marcia Hiriart5, Roberto Medina-Santillán6, María del Carmen Castillo-Hernandez6, Nahum Méndez-Sánchez7, Misael Uribe7, Nimbe Torres3. 1. Departamento de Cirugía Experimental, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City. Mexico; Departamento de Posgrado e Investigación, Instituto Politécnico Nacional, Escuela Superior de Medicina, Mexico City. Mexico. 2. Departamento de Cirugía Experimental, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City. Mexico. 3. Departamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City. Mexico. 4. Departamento de Patología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City. Mexico. 5. Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City. Mexico. 6. Departamento de Posgrado e Investigación, Instituto Politécnico Nacional, Escuela Superior de Medicina, Mexico City. Mexico. 7. Liver Research Unit. Medica Sur Clinic & Foundation. Mexico City, Mexico.
Abstract
BACKGROUND: The study of NAFLD in humans has several limitations. Using murine models helps to understand disease pathogenesis. AIM: Evaluate the impact of 4 different diets in the production of NAFLD with emphasis on a combined high-fat plus sustained high sucrose consumption. MATERIAL AND METHODS: Eight week-old male Wistar rats were divided in four groups and fed for 90 days with the following diets: 1) Control chow diet (C); 2) High-fat cholesterol diet (HFC) + 5% sucrose in drinking water. 3) High-fat cornstarch diet (HFCO) + 5% sucrose in drinking water. 4) Chow diet + 20% sucrose in drinking water (HSD). Metabolic changes, leptin levels, liver histology, hepatic and plasma lipid composition, fasting plasma glucose and insulin and liver gene expression of FAS, SREBP-1 and PPAR-α were evaluated. RESULTS: The HFC diet had the highest grade of steatosis (grade 2 of 3) and HSD showed also steatosis (grade 1). Liver weight TG and colesterol concentrations in liver were greater in the HFC diet. There were no increased levels of iron in the liver. Rats in HFC gained significantly more weight (P < 0.001). All experimental groups showed fasting hyperglycemia. HFC had the highest glucose level (158.5 ± 7 mg/dL) (P < 0.005). The HSD and the HFCO diets developed also hyperglycemia. HSD had significantly higher fasting hyperinsulinemia. Serum leptin was higher in the HFC diet (p = 0.001). In conclusion, the HFC diet with combination of high fat and high sucrose is more effective in producing NAFLD compared with a high sucrose diet only.
BACKGROUND: The study of NAFLD in humans has several limitations. Using murine models helps to understand disease pathogenesis. AIM: Evaluate the impact of 4 different diets in the production of NAFLD with emphasis on a combined high-fat plus sustained high sucrose consumption. MATERIAL AND METHODS: Eight week-old male Wistar rats were divided in four groups and fed for 90 days with the following diets: 1) Control chow diet (C); 2) High-fat cholesterol diet (HFC) + 5% sucrose in drinking water. 3) High-fat cornstarch diet (HFCO) + 5% sucrose in drinking water. 4) Chow diet + 20% sucrose in drinking water (HSD). Metabolic changes, leptin levels, liver histology, hepatic and plasma lipid composition, fasting plasma glucose and insulin and liver gene expression of FAS, SREBP-1 and PPAR-α were evaluated. RESULTS: The HFC diet had the highest grade of steatosis (grade 2 of 3) and HSD showed also steatosis (grade 1). Liver weight TG and colesterol concentrations in liver were greater in the HFC diet. There were no increased levels of iron in the liver. Rats in HFC gained significantly more weight (P < 0.001). All experimental groups showed fasting hyperglycemia. HFC had the highest glucose level (158.5 ± 7 mg/dL) (P < 0.005). The HSD and the HFCO diets developed also hyperglycemia. HSD had significantly higher fasting hyperinsulinemia. Serum leptin was higher in the HFC diet (p = 0.001). In conclusion, the HFC diet with combination of high fat and high sucrose is more effective in producing NAFLD compared with a high sucrose diet only.
Authors: Gonzalo Torres-Villalobos; Nashla Hamdan-Pérez; Andrea Díaz-Villaseñor; Armando R Tovar; Ivan Torre-Villalvazo; Guillermo Ordaz-Nava; Sofía Morán-Ramos; Lilia G Noriega; Braulio Martínez-Benítez; Alejandro López-Garibay; Samuel Torres-Landa; Juan C Ceballos-Cantú; Claudia Tovar-Palacio; Elizabeth Figueroa-Juárez; Marcia Hiriart; Roberto Medina-Santillán; Carmen Castillo-Hernández; Nimbe Torres Journal: Physiol Rep Date: 2016-09
Authors: Malinalli Brianza-Padilla; Roxana Carbó; Julio C Arana; Gonzalo Vázquez-Palacios; Martha A Ballinas-Verdugo; Guillermo C Cardoso-Saldaña; Adán G Palacio; Yaneli Juárez-Vicuña; Fausto Sánchez; Eduardo Martínez-Martínez; Fengyang Huang; Fausto Sánchez-Muñoz; Rafael Bojalil Journal: Biomed Res Int Date: 2016-11-24 Impact factor: 3.411