title: High dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.
abstract: 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 regimen of high-fructose and high-salt diet (HFS) for 10 more weeks, while the other groups were fed with their respective diets. Animals were then euthanized and their blood and liver were examined. Fasting plasma glucose was found to be significantly higher (approximately 50%) in fructose-fed rats than in the control and HS rats, whereas fat liver also differed in these animals, producing steatosis. Feeding fructose-fed rats with the high-salt diet triggered hyperinsulinemia and lowered insulin sensitivity, which led to increased levels of serum sodium compared to the HS group. This resulted in membrane perturbation, which in the presence of steatosis potentially enhanced hepatic lipid peroxidation, thereby decreasing the level of antioxidant defenses, as shown by GSH/GSSG ratio (HFS rats, 7.098±2.1 versus CON rats, 13.2±6.1) and superoxide dismutase (HFS rats, 2.1±0.05 versus CON rats, 2.3±0.1%), and catalase (HFS rats, 526.6±88.6 versus CON rats, 745.8±228.7 U/mg ptn) activities. Our results indicate that consumption of a salt-rich diet by insulin-resistant rats may lead to regulation of sodium reabsorption, worsening hepatic lipid peroxidation associated with impaired antioxidant defenses.
authors.affiliation: Research in Biological Sciences - NUPEB, Federal University of Ouro Preto, Minas Gerais, Brazil. Electronic address: w.dornas@ig.com.br.
authors.forename: Waleska Claudia
authors.initials: WC
authors.lastname: Dornas
authors.forename: Wanderson Geraldo
authors.initials: WG
authors.lastname: de Lima
authors.forename: Rinaldo Cardoso
authors.initials: RC
authors.lastname: dos Santos
authors.forename: Joyce Ferreira da Costa
authors.initials: JF
authors.lastname: Guerra
authors.forename: Melina Oliveira
authors.initials: MO
authors.lastname: de Souza
authors.forename: Maísa
authors.initials: M
authors.lastname: Silva
authors.forename: Lorena
authors.initials: L
authors.lastname: Souza e Silva
authors.forename: Mirla Fiuza
authors.initials: MF
authors.lastname: Diniz
authors.forename: Marcelo Eustáquio
authors.initials: ME
authors.lastname: Silva
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002374:Catalase / Q000378:metabolism; D005215:Fasting; D005632:Fructose / Q000008:administration & dosage*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D011916:Rats, Inbred F344; D012982:Sodium, Dietary / Q000008:administration & dosage* / Q000009:adverse effects; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D007328:Insulin; D012982:Sodium, Dietary; D017392:Thiobarbituric Acid Reactive Substances; D005632:Fructose; D002374:Catalase; D013482:Superoxide Dismutase
keywords: ALT; AST; Alanine aminotransferase; Aspartate aminotransferase; CAT; Catalase; GFR; GPx; GSH; GSSG; Glomerular filtration rate; Glutathione peroxidase (GPx); HOMA; Homeostasis model assessment; O(2)(−); Oxidized glutathione; ROS; Reactive oxygen species; Reduced glutathione; SOD; Superoxide anions; Superoxide dismutase; TBARS; Thiobarbituric acid reactive substances; antioxidant defenses; fructose-fed rats; high-salt diet; oxidative stress; steatosis