title: Effect of insulin and growth hormone on rat heart and liver oxidative stress in control and caloric restricted animals.
abstract: In order to know if insulin-like signalling is involved in the control of oxidative stress in mammalian tissues in relation to aging, ad libitum-fed and caloric restricted Wistar rats were treated during 2 weeks with GH and insulin. The most consistent effect of the hormonal treatments was an increase in plasma IGF-1 levels. Caloric restriction during 6 weeks decreased ROS generation and oxidative DNA damage in heart mitochondria and this was reversed by insulin treatment. The decrease in oxidative damage to liver nuclear DNA induced by caloric restriction was also reversed by GH and insulin. In the liver, however, insulin and GH decreased mitochondrial ROS generation while they increased oxidative damage to mitochondrial DNA. GH and insulin decreased three different markers of oxidative modification of liver proteins, while they increased lipoxidation-dependent markers. This last result is related to the increase in phospholipid unsaturation induced in the liver by both hormones. The results suggest that the idea that insulin-like signalling controls oxidative stress in mammals cannot be generalized since both prooxidant and protective effects of GH and insulin are observed depending on the particular parameter and tissue selected.
authors.affiliation: Department of Animal Physiology-II, Faculty of Biology, Complutense University, Madrid, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Sanz
authors.forename: R
authors.initials: R
authors.lastname: Gredilla
authors.forename: R
authors.initials: R
authors.lastname: Pamplona
authors.forename: M
authors.initials: M
authors.lastname: Portero-Otín
authors.forename: E
authors.initials: E
authors.lastname: Vara
authors.forename: J A F
authors.initials: JA
authors.lastname: Tresguerres
authors.forename: G
authors.initials: G
authors.lastname: Barja
mesh_terms: D000367:Age Factors; D000818:Animals; D031204:Caloric Restriction; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000187:drug effects / Q000378:metabolism; D013006:Growth Hormone / Q000097:blood / Q000494:pharmacology*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D004272:DNA, Mitochondrial; D007004:Hypoglycemic Agents; D007328:Insulin; D010743:Phospholipids; D017382:Reactive Oxygen Species; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone