Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity
نویسندگان
چکیده
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.
منابع مشابه
Zataria multiflora increases insulin sensitivity and PPARγ gene expression in high fructose fed insulin resistant rats
Objective(s):In insulin resistance, the insulin action in liver, muscles and adipocytes decreases and result in hyperglycemia, dyslipidemia and hyperinsulinemia. In this study we evaluate the effect of Zataria multiflora extract on insulin sensitivity in high fructose fed insulin resistant rats, since this extract was shown antihyperglycemic effect in streptozotocin induced diabetes in rats. ...
متن کاملBerberis integerrima ameliorates insulin resistance in high- fructose-fed insulin-resistant rats
Objective(s): This study was aimed to investigate the effect of Berberis integerrima (B. integerrima) extract on insulin sensitivity in high-fructose-fed insulin-resistant rats. Materials and Methods: Experimental rats were randomly divided into two groups: the control group was fed a regular chow diet while other group fed with a high-fructose diet for 8 weeks. After the first six weeks, the a...
متن کاملHigh dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.
In this study we investigated the hypothesis that a high-salt diet to hyperinsulinemic rats might impair antioxidant defense owing to its involvement in the activation of sodium reabsorption to lead to higher oxidative stress. Rats were fed a standard (CON), a high-salt (HS), or a high-fructose (HF) diet for 10 weeks after which, 50% of the animals belonging to the HF group were switched to a r...
متن کاملThe Effects of Simvastatin on Free Fatty Acids Profile in Fructose-fed Insulin Resistant Rats
Backgrounds: Type 2 diabetes mellitus is the most common metabolic disease and free fatty acids, as signaling molecules, can play a crucial role in the development of it. Different free fatty acids, through various cell membrane receptors, induce different effects on metabolic pathways and thereby affect insulin sensitivity. Simvastatin is a cholesterol decreasing drug prescrib...
متن کاملEffect of Vanadyl Sulfate on Fructose-Induced Insulin Resistance Rat
Insulin resistance syndrome, also referred to as the metabolic syndrome or syndrome X, refers to a constellation of common metabolic and cardiovascular disorders (e.g. obesity, type 2 diabetes mellitus, hypertension, and dyslipidemia), which are all cardiovascular risk factors. Insulin resistance can be induced by fructose-rich diet in rats. We investigated the effect of vanadyl sulfate (0.2 mg...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 9 شماره
صفحات -
تاریخ انتشار 2012