Open Access Open Badges Research article

Little effects of Insulin-like Growth Factor-I on testicular atrophy induced by hypoxia

Fernando Diez-Caballero1, Inma Castilla-Cortázar23*, Maria Garcia-Fernandez2, Juan Enrique Puche23, Matias Diaz-Sanchez1, Amelia Diaz Casares3, M Aurelia Aliaga-Montilla1, Coronación Rodriguez-Borrajo3 and Salvador Gonzalez-Barón2

Author Affiliations

1 Departments of Physiology and Urology. University of Navarra. Pamplona, Spain

2 Department of Human Physiology. School of Medicine. University of Málaga, Spain

3 Department of Human Physiology. School of Medicine. University San Pablo-CEU, Spain

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BMC Urology 2006, 6:4  doi:10.1186/1471-2490-6-4

Published: 21 February 2006



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.


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 μg.100 g, sc.) for 28d. 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.


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 signifincantly 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).


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 Syndrom or liver cirrhosis).