title: Hepatic oxidative stress in fructose-induced fatty liver is not caused by sulfur amino acid insufficiency.
abstract: Fructose-sweetened liquid consumption is associated with fatty liver and oxidative stress. In rodent models of fructose-mediated fatty liver, protein consumption is decreased. Additionally, decreased sulfur amino acid intake is known to cause oxidative stress. Studies were designed to test whether oxidative stress in fructose-sweetened liquid-induced fatty liver is caused by decreased ad libitum solid food intake with associated inadequate sulfur amino acid intake. C57BL6 mice were grouped as: control (ad libitum water), fructose (ad libitum 30% fructose-sweetened liquid), glucose (ad libitum 30% glucose-sweetened water) and pair-fed (ad libitum water and sulfur amino acid intake same as the fructose group). Hepatic and plasma thiol-disulfide antioxidant status were analyzed after five weeks. Fructose- and glucose-fed mice developed fatty liver. The mitochondrial antioxidant protein, thioredoxin-2, displayed decreased abundance in the liver of fructose and glucose-fed mice compared to controls. Glutathione/glutathione disulfide redox potential (E(h)GSSG) and abundance of the cytoplasmic antioxidant protein, peroxiredoxin-2, were similar among groups. We conclude that both fructose and glucose-sweetened liquid consumption results in fatty liver and upregulated thioredoxin-2 expression, consistent with mitochondrial oxidative stress; however, inadequate sulfur amino acid intake was not the cause of this oxidative stress.
authors.affiliation: Division of Gastroenterology, Hepatology and Nutrition, Emory Children's Center, Emory University School of Medicine, Atlanta, GA 30322, USA. sachin.kunde@helendevoschildrens.org
authors.forename: Sachin S
authors.initials: SS
authors.lastname: Kunde
authors.forename: James R
authors.initials: JR
authors.lastname: Roede
authors.forename: Miriam B
authors.initials: MB
authors.lastname: Vos
authors.forename: Michael L
authors.initials: ML
authors.lastname: Orr
authors.forename: Young-Mi
authors.initials: YM
authors.lastname: Go
authors.forename: Youngja
authors.initials: Y
authors.lastname: Park
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Ziegler
authors.forename: Dean P
authors.initials: DP
authors.lastname: Jones
mesh_terms: D000603:Amino Acids, Sulfur / Q000008:administration & dosage* / Q000172:deficiency; D000818:Animals; D001681:Biological Assay; D015153:Blotting, Western; D016022:Case-Control Studies; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000139:chemically induced / Q000378:metabolism*; D005632:Fructose / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress / Q000502:physiology; D054464:Peroxiredoxins / Q000378:metabolism; D013549:Sweetening Agents / Q000494:pharmacology*; D013879:Thioredoxins / Q000378:metabolism
chemical_list: D000603:Amino Acids, Sulfur; D013549:Sweetening Agents; C516112:Txn2 protein, mouse; D005632:Fructose; D013879:Thioredoxins; D054464:Peroxiredoxins; D005947:Glucose