Changes induced by a fructose-rich diet on hepatic metabolism and the antioxidant system

FRANCINI F.; CASTRO MC; SCHINELLA G; GARCIA ME; MAIZTEGUI B; RASCHIA A; GAGLIARDINO JJ; MASSA ML

LIFE SCIENCES

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2010 vol. 86 p. 965 - 971

0024-3205

Aims: to evaluate the effect of a fructose-rich diet (FRD) for 3 weeks, upon gene expression, protein and activity levels of liver antioxidant system and carbohydrate metabolism. Main methods: we measured serum glucose (fasting and after a glucose load), triglyceride and insulin levels. In liver we measured gene and protein expression and enzyme activity of catalase (CAT), CuZn-superoxide dismutase (CuZnSOD) and glutathione peroxidase (GSHPx); reduced glutathione (GSH); protein carbonyl content;  TBARS content and microsomal membrane susceptibility to lipid peroxidation; glucokinase (GK), glucose-6-phosphatase (G-6-Pase) and glucose-6-phosphate dehydrogenase (G-6-PDH) activity; and glycogen, pyruvate, lactate and triglyceride content. Key findings: similar body weights and caloric intake were recorded in both groups. FRD rats had higher serum glucose, insulin and triglyceride levels, molar insulin:glucose ratio and HOMA-IR values and impaired glucose tolerance, whereas relative gene expression levels of CAT, CuZnSOD and GSHPx were significantly lower. CAT and CuZnSOD protein expression, CAT activity and GSH content were also lower while protein carbonyl content was higher. No differences were recorded in CuZnSOD, MnSOD and GSHPx activity, TBARS content, and membrane susceptibility to lipid peroxidation. Glycogen, lactate and triglyceride content and GK, G-6-Pase and G-6-PDH activity were significantly higher in FRD rats. Significance: these data show that in the presence of oxidative stress, the liver exhibits changes in carbohydrate and lipid metabolic pathways that would decrease ROS production and its deleterious effect, thus suffering little impact on specific antioxidant mechanisms. This knowledge could facilitate the design and implementation of strategies to prevent oxidative stress-induced liver damage.