title: Iron Deprivation May Enhance Insulin Receptor and Glut4 Transcription in Skeletal Muscle of Adult Rats.
abstract: OBJECTIVE
  Considering that phenotype related to iron overload associated with pathological conditions differs from that caused by dietary iron excess, our study set out to evaluate the impact of dietary iron restriction and dietary iron supplementation on oxidative stress and functional outcome in adult, healthy rats.
  
  
  METHODS
  adult rats were divided into the three groups and fed diets containing 10, 35 or 350 mg/kg iron (restricted-diet, control-diet and supplemented- diet groups, respectively) for 78 days. Hematological variables, fasting blood glucose, hepatic enzyme activity and C-reactive protein levels were analyzed. Iron and glycogen concentrations in liver and skeletal muscle were determined. The extent of tissue damage caused by either dietary iron restriction or iron supplementation was accessed by measuring malondialdehyde, carbonyl, NADPH oxidase, glutathione peroxidase, glutathione reductase and glutathione-s-transferase in various tissues. The mRNA expression levels of insulin receptor, glucose transporter 4 and p53 were also determined.
  
  
  RESULTS
  Fasting blood glucose values trended toward a decrease by dietary iron restriction, moreover, hepatic glycogen content decreased with concomitant increases in skeletal muscle. In addition, dietary iron restriction resulted in a twofold increase in mRNA expression of Insr and fourfold increase in Glut4 expression in skeletal muscle. Although the dietary iron restriction did not affect body iron status, it caused hepatic low oxidative damages. However, high liver NADPH oxidase activity and increased levels of protein oxidation in muscle were observed. Chronic feeding of high iron diet induces iron overload and resulted in elevated levels of stress markers in tissues.
  
  
  CONCLUSIONS
  Dietary iron deprivation may improve insulin receptor and glucose transporter transcription in muscle; however, our results show that dietary iron restriction can prevent and/or promote oxidative damage in a tissue-specific manner, emphasizing the importance of maintaining optimal iron intake.
authors.affiliation: Azadeh Mehdad, Laboratory of Molecular biophysic, Instituto of Biology, Dep. Cellular Biology, University of Brasilia (UnB) Brazil, azadehmehdad@gmail.com.
authors.forename: A
authors.initials: A
authors.lastname: Mehdad
authors.forename: N A
authors.initials: NA
authors.lastname: Campos
authors.forename: S Fernandes
authors.initials: SF
authors.lastname: Arruda
authors.forename: E Machado de Almeida
authors.initials: EM
authors.lastname: Siqueira
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D004032:Diet; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D019266:Iron, Dietary / Q000378:metabolism*; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics
chemical_list: D001786:Blood Glucose; D051275:Glucose Transporter Type 4; D019266:Iron, Dietary; D016159:Tumor Suppressor Protein p53; D006003:Glycogen; D002097:C-Reactive Protein; D007501:Iron; D019255:NADPH Oxidases; D011972:Receptor, Insulin