Dornas, Waleska Claudia AmaralLima, Wanderson Geraldo deSantos, Rinaldo Cardoso dosSouza, Melina Oliveira deSilva, MaísaDiniz, Mirla FiuzaSilva, Marcelo Eustáquio2015-03-132015-03-132012DORNAS, 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: <http://www.nutritionandmetabolism.com/content/9/1/63>. Acesso em: 08 nov. 2014.1743-7075http://www.repositorio.ufop.br/handle/123456789/4626Paraoxonase 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.en-USFructose fed ratsHigh salt dietParaoxonaseAtherosclerosisArtigo publicado em periodicoThis 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. Fonte: o próprio artigo.https://doi.org/10.1186/1743-7075-9-63