Pituitary and testicular function in growth hormone receptor gene knockout mice
Pituitary and testicular function in growth hormone receptor gene knockout mice
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DOI：
10.1210/en.140.3.1082
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发表时间：
1999-03-01
期刊：
影响因子：
4.8
通讯作者：
Kopchick, JJ
中科院分区：
文献类型：
--
作者：
Chandrashekar, V;Bartke, A;Kopchick, JJ
GH在控制垂体和睾丸功能中的作用知之甚少。最近产生了GH受体基因敲除（GHR-KO）小鼠。由于这些小鼠是评估GH和胰岛素样生长因子-I（IGF-I）效应影响的良好实验动物，因此进行了本研究。测试年轻成年雄性GHR-KO小鼠及其正常同胞的生育力，随后用盐水或盐水中的GnRH（lng/g BW）注射。15分钟后，通过心脏穿刺获得血液。通过RLAs测定血浆IGF-I、PRL、LH和睾酮浓度。此外，在体外评价了睾丸睾酮对LH处理的反应。结果表明，GH受体（GHR）的缺乏与血浆PRL水平的升高有关（P < 0.005），而循环IGF-I检测不到。尽管GHR-KO小鼠的基础血浆LH水平与其正常同胞相似，但GnRH治疗的循环LH反应显著减弱（P < 0.001）。血浆睾酮水平不受GHR基因破坏的影响。但GHR基因敲除小鼠睾丸的基础（P < 0.01）和LH刺激（P < 0.001）睾酮释放均减少。GHR-KO雄性小鼠的生育率也降低。这些结果表明，缺乏生长激素受体（生长激素抵抗和IGF-I分泌缺乏）诱导高泌乳素血症，改变了促性腺激素释放激素对LH分泌以及睾丸功能的影响。因此，GH和IGF-I影响雄性小鼠的垂体和性腺功能。
The role of GH in the control of pituitary and testicular function is poorly understood. GH receptor gene knockout (GHR-KO) mice were recently produced. As these mice are good experimental animals to assess the influence of the effects of GH and insulin-like growth factor-I (IGF-I), the present studies were undertaken. Young adult male GHR-KO mice and their normal siblings were tested for fertility and subsequently injected tip) with saline or GnRH (1 ng/g BW) in saline. Fifteen minutes later, blood was obtained via heart puncture. Plasma IGF-I, PRL, LH, and testosterone concentrations were measured by RLAs. In addition, the testicular testosterone response to LH treatment was evaluated in vitro. The results indicate that the absence of GH receptors (GHRs) was associated with an increase (P < 0.005) in plasma PRL levels, and circulating IGF-I was not detectable. Although the basal plasma LH levels were similar in GHR-KO mice relative to those in their normal siblings, the circulating LH response to GnRH treatment was significantly (P < 0.001) attenuated. Plasma testosterone levels were unaffected by disruption of the GHR gene. However, basal (P < 0.01) and LH-stimulated (P < 0.001)testosterone release from the isolated testes of GHR-KO mice were decreased. The rate of fertility in GHR-KO male mice was also reduced. These results indicate that the lack of GHRs (with GH resistance and lack of IGF-I secretion) induces hyperprolactinemia and alters the effect of GnRH on LH secretion as well as testicular function. Thus, GH and IGF-I influence pituitary and gonadal functions in male mice.