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Title: Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity.
Authors: Dornas, Waleska Claudia Amaral
Lima, Wanderson Geraldo de
Santos, Rinaldo Cardoso dos
Souza, Melina Oliveira de
Silva, Maísa
Diniz, Mirla Fiuza
Silva, Marcelo Eustáquio
Keywords: Fructose fed rats
High salt diet
Issue Date: 2012
Citation: DORNAS, W. C. et al. Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity. Nutrition & Metabolism, v. 9, p. 63, 2012. Disponível em: <>. Acesso em: 08 nov. 2014.
Abstract: 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.
ISSN: 1743-7075
metadata.dc.rights.license: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fonte: o próprio artigo.
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