Diez-Caballero Fernando, Castilla-Cortázar Inma, Garcia-Fernandez Maria, Puche Juan Enrique, Diaz-Sanchez Matias, Casares Amelia Diaz, Aliaga-Montilla M Aurelia, Rodriguez-Borrajo Coronación, Gonzalez-Barón Salvador
Department of Physiology, University of Navarra, Pamplona, Spain.
BMC Urol. 2006 Feb 21;6:4. doi: 10.1186/1471-2490-6-4.
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 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.
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).
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).
补充胰岛素样生长因子-I（IGF-I）可恢复与晚期肝硬化相关的睾丸萎缩，晚期肝硬化是一种IGF-I缺乏的病症。本研究的目的是评估IGF-I对无肝脏疾病、血清IGF-I水平正常的缺血性睾丸萎缩（AT）大鼠的影响。
在11周内通过肾上腺素（1、2mg/Kg阴囊内注射，每周5次）诱导睾丸萎缩。然后，将睾丸萎缩（AT）大鼠分为两组（每组n = 10）：接受皮下注射生理盐水的未治疗大鼠（AT），以及接受IGF-I（2μg·100g体重-1·天-1，皮下注射）治疗28天的AT+IGF组。同时研究健康对照（CO，n = 10）。在第29天处死动物。评估垂体-性腺轴、IGF-I和IGFBPs水平、睾丸形态学和组织病理学、免疫组织化学研究以及抗氧化酶活性磷脂氢过氧化物谷胱甘肽过氧化物酶（PHGPx）。
与对照组相比，AT大鼠的睾丸大小和重量减小，出现组织学上的睾丸萎缩，细胞增殖和转铁蛋白表达降低，低剂量IGF-I可使所有这些改变略有改善。IGF-I治疗显著增加了类固醇生成和PHGPx活性（p < 0.05）。有趣的是，用IGF-I治疗的睾丸萎缩大鼠的血浆IGF-I并未增加，而降低IGF-I可用性的IGFBP3水平在该组中升高（p < 0.05）。
在无IGF-I缺乏的缺氧性睾丸萎缩中，IGF治疗仅产生部分效果。这些发现表明，仅当性腺功能减退与IGF-I缺乏症（如拉伦综合征或肝硬化）相关时，IGF-I治疗才似乎是一种合适的治疗方法。
