Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence
Autor: | Fabiana Rodrigues Silva Gasparin, Adelar Bracht, Fernando Carreño, Maria Raquel Marçal Natali, Cristiane Vizioli de Castro Ghizoni, Eduardo Hideo Gilglioni, Jorgete Constantin, Karina Sayuri Utsunomiya, Márcio Mendes Rocha, Emy Luiza Ishii-Iwamoto, Antonio Sueiti Maeda Júnior, Solange Marta Franzói de Moraes, Rodrigo Polimeni Constantin |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty obesity high caloric density food 030209 endocrinology & metabolism Cafeteria lcsh:TX341-641 Glucagon Article 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Insulin resistance Oxygen Consumption Internal medicine NAFLD Pyruvic Acid medicine Animals Lactic Acid Rats Wistar Nutrition and Dietetics Glycogen biology Fatty liver Fatty Acids Gluconeogenesis Feeding Behavior medicine.disease biology.organism_classification Diet Rats Fatty Liver 030104 developmental biology Endocrinology Glucose chemistry Pyruvic acid hyperglycemia Steatosis hemodynamic changes Energy Intake lcsh:Nutrition. Foods and food supply glucose production Food Science |
Zdroj: | Nutrients Nutrients, Vol 10, Iss 11, p 1571 (2018) Volume 10 Issue 11 |
ISSN: | 2072-6643 |
Popis: | Gluconeogenesis overstimulation due to hepatic insulin resistance is the best-known mechanism behind elevated glycemia in obese subjects with hepatic steatosis. This suggests that glucose production in fatty livers may differ from that of healthy livers, also in response to other gluconeogenic determinant factors, such as the type of substrate and modulators. Thus, the aim of this study was to investigate the effects of these factors on hepatic gluconeogenesis in cafeteria diet-induced obese adult rats submitted to a cafeteria diet at a young age. The livers of the cafeteria group exhibited higher gluconeogenesis rates when glycerol was the substrate, but lower rates were found when lactate and pyruvate were the substrates. Stearate or glucagon caused higher stimulations in gluconeogenesis in cafeteria group livers, irrespective of the gluconeogenic substrates. An increased mitochondrial NADH/NAD+ ratio and a reduced rate of 14CO2 production from [14C] fatty acids suggested restriction of the citric acid cycle. The higher glycogen and lipid levels were possibly the cause for the reduced cellular and vascular spaces found in cafeteria group livers, likely contributing to oxygen consumption restriction. In conclusion, specific substrates and gluconeogenic modulators contribute to a higher stimulation of gluconeogenesis in livers from the cafeteria group. |
Databáze: | OpenAIRE |
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