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Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet

BACKGROUND: Metabolic syndrome is associated with an increased risk of cardiovascular and hepatic complications. Oxidative stress in metabolic tissues has emerged as a universal feature of metabolic syndrome and its co-morbidities. We aimed to develop a rapidly and easily induced model of metabolic...

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Autores principales: Auberval, Nathalie, Dal, Stéphanie, Bietiger, William, Pinget, Michel, Jeandidier, Nathalie, Maillard-Pedracini, Elisa, Schini-Kerth, Valérie, Sigrist, Séverine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424531/
https://www.ncbi.nlm.nih.gov/pubmed/25960774
http://dx.doi.org/10.1186/1758-5996-6-130
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author Auberval, Nathalie
Dal, Stéphanie
Bietiger, William
Pinget, Michel
Jeandidier, Nathalie
Maillard-Pedracini, Elisa
Schini-Kerth, Valérie
Sigrist, Séverine
author_facet Auberval, Nathalie
Dal, Stéphanie
Bietiger, William
Pinget, Michel
Jeandidier, Nathalie
Maillard-Pedracini, Elisa
Schini-Kerth, Valérie
Sigrist, Séverine
author_sort Auberval, Nathalie
collection PubMed
description BACKGROUND: Metabolic syndrome is associated with an increased risk of cardiovascular and hepatic complications. Oxidative stress in metabolic tissues has emerged as a universal feature of metabolic syndrome and its co-morbidities. We aimed to develop a rapidly and easily induced model of metabolic syndrome in rats to evaluate its impact on plasma and tissue oxidative stress. MATERIALS AND METHODS: Metabolic syndrome was induced in rats using a high-fat diet (HFD), and these rats were compared to rats fed a normal diet (ND) for 2 months. Metabolic control was determined by measuring body weight, blood glucose, triglycerides, lipid peroxidation and protein carbonylation in plasma. Insulinemia was evaluated through the measure of C-peptide. Histological analysis was performed on the pancreas, liver and blood vessels. RESULTS: After 2 months, the HFD induced an increase in body weight, insulin and triglycerides. Liver steatosis was also observed in the HFD group, which was associated with an increase in glycogen storage. In the pancreas, the HFD induced islet hyperplasia. Tissue oxidative stress was also increased in the liver, pancreas and blood vessels, but plasma oxidative stress remained unchanged. CONCLUSION: This paper reports the development of a fast and easy model of rat metabolic syndrome associated with tissue oxidative stress. This model may be a good tool for the biological validation of drugs or antioxidants to limit or prevent the complications of metabolic syndrome.
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spelling pubmed-44245312015-05-09 Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet Auberval, Nathalie Dal, Stéphanie Bietiger, William Pinget, Michel Jeandidier, Nathalie Maillard-Pedracini, Elisa Schini-Kerth, Valérie Sigrist, Séverine Diabetol Metab Syndr Research BACKGROUND: Metabolic syndrome is associated with an increased risk of cardiovascular and hepatic complications. Oxidative stress in metabolic tissues has emerged as a universal feature of metabolic syndrome and its co-morbidities. We aimed to develop a rapidly and easily induced model of metabolic syndrome in rats to evaluate its impact on plasma and tissue oxidative stress. MATERIALS AND METHODS: Metabolic syndrome was induced in rats using a high-fat diet (HFD), and these rats were compared to rats fed a normal diet (ND) for 2 months. Metabolic control was determined by measuring body weight, blood glucose, triglycerides, lipid peroxidation and protein carbonylation in plasma. Insulinemia was evaluated through the measure of C-peptide. Histological analysis was performed on the pancreas, liver and blood vessels. RESULTS: After 2 months, the HFD induced an increase in body weight, insulin and triglycerides. Liver steatosis was also observed in the HFD group, which was associated with an increase in glycogen storage. In the pancreas, the HFD induced islet hyperplasia. Tissue oxidative stress was also increased in the liver, pancreas and blood vessels, but plasma oxidative stress remained unchanged. CONCLUSION: This paper reports the development of a fast and easy model of rat metabolic syndrome associated with tissue oxidative stress. This model may be a good tool for the biological validation of drugs or antioxidants to limit or prevent the complications of metabolic syndrome. BioMed Central 2014-11-28 /pmc/articles/PMC4424531/ /pubmed/25960774 http://dx.doi.org/10.1186/1758-5996-6-130 Text en © Auberval et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Auberval, Nathalie
Dal, Stéphanie
Bietiger, William
Pinget, Michel
Jeandidier, Nathalie
Maillard-Pedracini, Elisa
Schini-Kerth, Valérie
Sigrist, Séverine
Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title_full Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title_fullStr Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title_full_unstemmed Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title_short Metabolic and oxidative stress markers in Wistar rats after 2 months on a high-fat diet
title_sort metabolic and oxidative stress markers in wistar rats after 2 months on a high-fat diet
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424531/
https://www.ncbi.nlm.nih.gov/pubmed/25960774
http://dx.doi.org/10.1186/1758-5996-6-130
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