title: Influence of dietary supplementation with dextrin or oligofructose on the hepatic redox balance in rats.
abstract: We assessed the impact of oligofructose (OFS) and dextrin (DEX) as diet supplements on hepatic redox state. Rats were fed either a 10% OFS or a 10% DEX supplemented diet for 9 wk. In the DEX diet group, the levels of hepatic protein carbonylation were decreased by 63%. Total glutathione and reduced glutathione (GSH) contents were reduced in the OFS and DEX diet groups by around 20%. DEX supplementation significantly reduced oxidized glutathione (GSSG) levels resulting in a 33% increase in the GSH/GSSG ratio. The activity of the hepatic antioxidant enzymes was not changed by either OFS or DEX supplementation. OFS supplementation caused a decrease in serum levels of triglycerides (36%), cholesterol (24%), HDL (16%) and LDL (17%). DEX supplementation only reduced triglycerides (32%) and urea (22%). Both diets increased serum levels of acetate by fivefold and propionate by twofold, but DEX diet decreased butyrate levels by 75%. Due to their different composition/structure these two dietary fibers affected metabolism in different ways. Diet supplementation with 10% DEX can potentially improve host health, by protecting the liver from protein carbonylation and by improving GSH/GSSG ratio and diet supplementation with 10% OFS can improve the lipid profile.
authors.affiliation: Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Porto, Porto, Portugal. cepinto@med.up.pt
authors.forename: Carina E P
authors.initials: CE
authors.lastname: Kozmus
authors.forename: Eduardo
authors.initials: E
authors.lastname: Moura
authors.forename: Maria P
authors.initials: MP
authors.lastname: Serrão
authors.forename: Helena
authors.initials: H
authors.lastname: Real
authors.forename: João T
authors.initials: JT
authors.lastname: Guimarães
authors.forename: Paula
authors.initials: P
authors.lastname: Guedes-de-Pinho
authors.forename: Barbara P
authors.initials: BP
authors.lastname: Duarte
authors.forename: Franklim
authors.initials: F
authors.lastname: Marques
authors.forename: Maria João
authors.initials: MJ
authors.lastname: Martins
authors.forename: Maria A
authors.initials: MA
authors.lastname: Vieira-Coelho
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003912:Dextrins / Q000627:therapeutic use*; D005232:Fatty Acids, Volatile / Q000097:blood; D005978:Glutathione / Q000378:metabolism; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008074:Lipoproteins / Q000097:blood; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008659:Metabolic Diseases / Q000517:prevention & control; D009844:Oligosaccharides / Q000627:therapeutic use*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D056692:Prebiotics; D050050:Protein Carbonylation; D011897:Random Allocation; D051381:Rats; D014280:Triglycerides / Q000097:blood; D014508:Urea / Q000097:blood
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D003912:Dextrins; D005232:Fatty Acids, Volatile; D000960:Hypolipidemic Agents; D008074:Lipoproteins; D009844:Oligosaccharides; D056692:Prebiotics; D014280:Triglycerides; C120489:oligofructose; D014508:Urea; D002784:Cholesterol; D005978:Glutathione