title: Little effects of insulin-like Growth Factor-I on testicular atrophy induced by hypoxia.
abstract: BACKGROUND
  Insulin-like Growth Factor-I (IGF-I) supplementation restores testicular atrophy associated with advanced liver cirrhosis that is a condition of IGF-I deficiency. The aim of this work was to evaluate the effect of IGF-I in rats with ischemia-induced testicular atrophy (AT) without liver disease and consequently with normal serum level of IGF-I.
  
  
  METHODS
  Testicular atrophy was induced by epinephrine (1, 2 mg/Kg intra-scrotal injection five times per week) during 11 weeks. Then, rats with testicular atrophy (AT) were divided into two groups (n = 10 each): untreated rats (AT) receiving saline sc, and AT+IGF, which were treated with IGF-I (2 microg.100 g b.w.(-1).day(-1), sc.) for 28 d. Healthy controls (CO, n = 10) were studied in parallel. Animals were sacrificed on day 29th. Hypophyso-gonadal axis, IGF-I and IGFBPs levels, testicular morphometry and histopathology, immuno-histochemical studies and antioxidant enzyme activity phospholipid hydroperoxide glutathione peroxidase (PHGPx) were assessed.
  
  
  RESULTS
  Compared to controls, AT rats displayed a reduction in testicular size and weight, with histological testicular atrophy, decreased cellular proliferation and transferrin expression, and all of these alterations were slightly improved by IGF-I at low doses. IGF-I therapy increased significantly steroidogenesis and PHGPx activity (p < 0.05). Interestingly, plasma IGF-I did not augment in rats with testicular atrophy treated with IGF-I, while IGFBP3 levels, that reduces IGF-I availability, was increased in this group (p < 0.05).
  
  
  CONCLUSIONS
  In testicular atrophy by hypoxia, condition without IGF-I deficiency, IGF-treatment induces only partial effects. These findings suggest that IGF-I therapy appears as an appropriate treatment in hypogonadism only when this is associated to conditions of IGF-I deficiency (such as Laron Syndrome or liver cirrhosis).
authors.affiliation: Department of Physiology, University of Navarra, Pamplona, Spain. fdcaballero@yahoo.com
authors.forename: Fernando
authors.initials: F
authors.lastname: Diez-Caballero
authors.forename: Inma
authors.initials: I
authors.lastname: Castilla-Cortázar
authors.forename: Maria
authors.initials: M
authors.lastname: Garcia-Fernandez
authors.forename: Juan Enrique
authors.initials: JE
authors.lastname: Puche
authors.forename: Matias
authors.initials: M
authors.lastname: Diaz-Sanchez
authors.forename: Amelia Diaz
authors.initials: AD
authors.lastname: Casares
authors.forename: M Aurelia
authors.initials: MA
authors.lastname: Aliaga-Montilla
authors.forename: Coronación
authors.initials: C
authors.lastname: Rodriguez-Borrajo
authors.forename: Salvador
authors.initials: S
authors.lastname: Gonzalez-Barón
mesh_terms: D000818:Animals; D001284:Atrophy; D049109:Cell Proliferation; D005979:Glutathione Peroxidase / Q000378:metabolism; D000860:Hypoxia / Q000473:pathology*; D007150:Immunohistochemistry; D018969:Insulin-Like Growth Factor Binding Proteins / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000494:pharmacology*; D007511:Ischemia / Q000378:metabolism / Q000473:pathology*; D008297:Male; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012671:Seminiferous Tubules / Q000473:pathology; D013737:Testis / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D014168:Transferrin / Q000032:analysis
chemical_list: D018969:Insulin-Like Growth Factor Binding Proteins; D018809:Proliferating Cell Nuclear Antigen; D014168:Transferrin; D007334:Insulin-Like Growth Factor I; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase