Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence
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 deter...
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MDPI AG
2018-10-01
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Series: | Nutrients |
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Online Access: | https://www.mdpi.com/2072-6643/10/11/1571 |
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Article |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Antonio Sueiti Maeda Júnior Jorgete Constantin Karina Sayuri Utsunomiya Eduardo Hideo Gilglioni Fabiana Rodrigues Silva Gasparin Fernando Olinto Carreño Solange Marta Franzói de Moraes Márcio Rocha Maria Raquel Marçal Natali Cristiane Vizioli de Castro Ghizoni Adelar Bracht Emy Luiza Ishii-Iwamoto Rodrigo Polimeni Constantin |
spellingShingle |
Antonio Sueiti Maeda Júnior Jorgete Constantin Karina Sayuri Utsunomiya Eduardo Hideo Gilglioni Fabiana Rodrigues Silva Gasparin Fernando Olinto Carreño Solange Marta Franzói de Moraes Márcio Rocha Maria Raquel Marçal Natali Cristiane Vizioli de Castro Ghizoni Adelar Bracht Emy Luiza Ishii-Iwamoto Rodrigo Polimeni Constantin Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence Nutrients obesity high caloric density food NAFLD glucose production hyperglycemia hemodynamic changes |
author_facet |
Antonio Sueiti Maeda Júnior Jorgete Constantin Karina Sayuri Utsunomiya Eduardo Hideo Gilglioni Fabiana Rodrigues Silva Gasparin Fernando Olinto Carreño Solange Marta Franzói de Moraes Márcio Rocha Maria Raquel Marçal Natali Cristiane Vizioli de Castro Ghizoni Adelar Bracht Emy Luiza Ishii-Iwamoto Rodrigo Polimeni Constantin |
author_sort |
Antonio Sueiti Maeda Júnior |
title |
Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence |
title_short |
Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence |
title_full |
Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence |
title_fullStr |
Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence |
title_full_unstemmed |
Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence |
title_sort |
cafeteria diet feeding in young rats leads to hepatic steatosis and increased gluconeogenesis under fatty acids and glucagon influence |
publisher |
MDPI AG |
series |
Nutrients |
issn |
2072-6643 |
publishDate |
2018-10-01 |
description |
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<sup>+</sup> ratio and a reduced rate of <sup>14</sup>CO<sub>2</sub> production from [<sup>14</sup>C] 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. |
topic |
obesity high caloric density food NAFLD glucose production hyperglycemia hemodynamic changes |
url |
https://www.mdpi.com/2072-6643/10/11/1571 |
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doaj-bdf88ae065dd4d0dbe75c82b9f4c9b562020-11-24T22:03:18ZengMDPI AGNutrients2072-66432018-10-011011157110.3390/nu10111571nu10111571Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon InfluenceAntonio Sueiti Maeda Júnior0Jorgete Constantin1Karina Sayuri Utsunomiya2Eduardo Hideo Gilglioni3Fabiana Rodrigues Silva Gasparin4Fernando Olinto Carreño5Solange Marta Franzói de Moraes6Márcio Rocha7Maria Raquel Marçal Natali8Cristiane Vizioli de Castro Ghizoni9Adelar Bracht10Emy Luiza Ishii-Iwamoto11Rodrigo Polimeni Constantin12Department of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Morphophysiological Sciences, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Morphophysiological Sciences, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Liver Metabolism, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Liver Metabolism, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilDepartment of Biochemistry, Laboratory of Biological Oxidations and Laboratory of Experimental Steatosis, State University of Maringá, Maringá 87020-900, Paraná, BrazilGluconeogenesis 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<sup>+</sup> ratio and a reduced rate of <sup>14</sup>CO<sub>2</sub> production from [<sup>14</sup>C] 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.https://www.mdpi.com/2072-6643/10/11/1571obesityhigh caloric density foodNAFLDglucose productionhyperglycemiahemodynamic changes |