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Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity
Paraoxonase 1 (PON1) is a HDL-associated esterase/lactonase and its activity is inversely related to the risk of cardiovascular diseases. The aim of the present study was to evaluate the effect of a high-salt diet on serum PON1 activity in fructose-fed insulin-resistant rats. Adult male Fischer rats...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407710/ https://www.ncbi.nlm.nih.gov/pubmed/22738670 http://dx.doi.org/10.1186/1743-7075-9-63 |
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author | Dornas, Waleska Cláudia de Lima, Wanderson Geraldo dos Santos, Rinaldo Cardoso de Souza, Melina Oliveira Silva, Maísa Diniz, Mirla Fiuza Silva, Marcelo Eustáquio |
author_facet | Dornas, Waleska Cláudia de Lima, Wanderson Geraldo dos Santos, Rinaldo Cardoso de Souza, Melina Oliveira Silva, Maísa Diniz, Mirla Fiuza Silva, Marcelo Eustáquio |
author_sort | Dornas, Waleska Cláudia |
collection | PubMed |
description | Paraoxonase 1 (PON1) is a HDL-associated esterase/lactonase and its activity is inversely related to the risk of cardiovascular diseases. The aim of the present study was to evaluate the effect of a high-salt diet on serum PON1 activity in fructose-fed insulin-resistant rats. Adult male Fischer rats were initially divided into two groups. Control (CON), which received a normal salt diet and drinking water throughout the study; high fructose (HF), which received a normal salt diet and 20% fructose supplemented drinking water. After 10 weeks, half of the animals from HF group were randomly switched to a high-salt diet and 20% fructose supplemented drinking water (HFS) for more 10 weeks. Serum PON1 activity was determined by synthetic substrate phenyl acetate. HFS rats showed markedly decreased PON1 activity (HFS rats, 44.3 ± 14.4 g/dL versus CON rats, 64.4 ± 13.3 g/dL, P < 0.05) as compared to controls. In parallel, the level of oxidative stress, as indicated by thiobarbituric acid reactive substances (TBARS), was increased in HFS rats by 1.2-fold in the liver in relation to controls and was negatively correlated with PON activity. Differential leukocyte counts in blood showed a significant change in lymphocytes and monocytes profile. In conclusion, these results show that PON1 activity is decreased in fructose-fed insulin-resistant rats on a high-salt diet, which may be associated with increased oxidative stress, leading to inflammation. |
format | Online Article Text |
id | pubmed-3407710 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-34077102012-07-30 Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity Dornas, Waleska Cláudia de Lima, Wanderson Geraldo dos Santos, Rinaldo Cardoso de Souza, Melina Oliveira Silva, Maísa Diniz, Mirla Fiuza Silva, Marcelo Eustáquio Nutr Metab (Lond) Brief Communication Paraoxonase 1 (PON1) is a HDL-associated esterase/lactonase and its activity is inversely related to the risk of cardiovascular diseases. The aim of the present study was to evaluate the effect of a high-salt diet on serum PON1 activity in fructose-fed insulin-resistant rats. Adult male Fischer rats were initially divided into two groups. Control (CON), which received a normal salt diet and drinking water throughout the study; high fructose (HF), which received a normal salt diet and 20% fructose supplemented drinking water. After 10 weeks, half of the animals from HF group were randomly switched to a high-salt diet and 20% fructose supplemented drinking water (HFS) for more 10 weeks. Serum PON1 activity was determined by synthetic substrate phenyl acetate. HFS rats showed markedly decreased PON1 activity (HFS rats, 44.3 ± 14.4 g/dL versus CON rats, 64.4 ± 13.3 g/dL, P < 0.05) as compared to controls. In parallel, the level of oxidative stress, as indicated by thiobarbituric acid reactive substances (TBARS), was increased in HFS rats by 1.2-fold in the liver in relation to controls and was negatively correlated with PON activity. Differential leukocyte counts in blood showed a significant change in lymphocytes and monocytes profile. In conclusion, these results show that PON1 activity is decreased in fructose-fed insulin-resistant rats on a high-salt diet, which may be associated with increased oxidative stress, leading to inflammation. BioMed Central 2012-06-27 /pmc/articles/PMC3407710/ /pubmed/22738670 http://dx.doi.org/10.1186/1743-7075-9-63 Text en Copyright ©2012 Dornas et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Brief Communication Dornas, Waleska Cláudia de Lima, Wanderson Geraldo dos Santos, Rinaldo Cardoso de Souza, Melina Oliveira Silva, Maísa Diniz, Mirla Fiuza Silva, Marcelo Eustáquio Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title | Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title_full | Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title_fullStr | Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title_full_unstemmed | Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title_short | Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
title_sort | salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity |
topic | Brief Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407710/ https://www.ncbi.nlm.nih.gov/pubmed/22738670 http://dx.doi.org/10.1186/1743-7075-9-63 |
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