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生长激素过表达通过对瘦素的作用破坏生殖状态。

Growth Hormone Overexpression Disrupts Reproductive Status Through Actions on Leptin.

作者信息

Chen Ji, Cao Mengxi, Zhang Aidi, Shi Mijuan, Tao Binbin, Li Yongming, Wang Yaping, Zhu Zuoyan, Trudeau Vance L, Hu Wei

机构信息

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.

Institute of Environment and Health, Jianghan University, Wuhan, China.

出版信息

Front Endocrinol (Lausanne). 2018 Mar 27;9:131. doi: 10.3389/fendo.2018.00131. eCollection 2018.

DOI:10.3389/fendo.2018.00131
PMID:29636726
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5880896/
Abstract

Growth and reproduction are closely related. Growth hormone (GH)-transgenic common carp exhibit accelerated growth and delayed reproductive development, which provides an amenable model to study hormone cross talk between the growth and reproductive axes. We analyzed the energy status and reproductive development in GH-transgenic common carp by using multi-tissue RNA sequencing, real-time-PCR, Western blotting, ELISA, immunofluorescence, and incubation. The expression of (glycogen synthase) and (insulin-like growth factor binding protein) as well as blood glucose concentrations are lower in GH-transgenic carp. (agouti-related protein 1) and (somatolactin ), which are related to appetite and lipid catabolism, are significantly higher in GH-transgenic carp. Low glucose content and increased appetite indicate disrupted metabolic and energy deprivation status in GH-transgenic carp. Meanwhile, the expression of genes, such as (gonadotropin-releasing hormone receptor 2), (gonadotropin hormone, alpha polypeptide), (follicle stimulating hormone, beta polypeptide), [luteinizing hormone, beta polypeptide] in the pituitary, (aromatase A) in the gonad, and (aromatase B) in the hypothalamus, are decreased in GH-transgenic carp. In contrast, pituitary (gonadotropin inhibitory hormone), (dopamine receptor D1), (dopamine receptor D3), and (dopamine receptor D4) exhibit increased expression, which were associated with the retarded reproductive development. Leptin receptor mRNA was detected by fluorescence hybridization in the pituitary including the pars intermedia and proximal pars distalis, suggesting a direct effect of leptin on LH. Recombinant carp Leptin protein was shown to stimulate pituitary expression, and ovarian germinal vesicle breakdown . In addition to neuroendocrine factors, we suggest that reduced hepatic leptin signaling to the pituitary might be part of the response to overexpression of GH and the resulting delay in puberty onset.

摘要

生长与繁殖密切相关。生长激素(GH)转基因鲤鱼生长加速但生殖发育延迟,这为研究生长轴与生殖轴之间的激素相互作用提供了一个合适的模型。我们通过多组织RNA测序、实时定量PCR、蛋白质免疫印迹、酶联免疫吸附测定、免疫荧光和孵育等方法分析了GH转基因鲤鱼的能量状态和生殖发育情况。GH转基因鲤鱼中糖原合酶和胰岛素样生长因子结合蛋白的表达以及血糖浓度较低。与食欲和脂质分解代谢相关的刺鼠相关蛋白1和生长抑素在GH转基因鲤鱼中显著升高。低葡萄糖含量和食欲增加表明GH转基因鲤鱼的代谢紊乱和能量剥夺状态。同时,GH转基因鲤鱼垂体中促性腺激素释放激素受体2、促性腺激素α亚基、促卵泡激素β亚基、促黄体生成素β亚基、性腺中芳香化酶A以及下丘脑芳香化酶B的基因表达均降低。相反,垂体中促性腺激素抑制激素、多巴胺受体D1、多巴胺受体D3和多巴胺受体D4的表达增加,这与生殖发育延迟有关。通过荧光原位杂交在包括垂体中间部和远侧部近端的垂体中检测到瘦素受体mRNA,提示瘦素对促黄体生成素有直接作用。重组鲤鱼瘦素蛋白可刺激垂体促黄体生成素的表达以及卵巢生发泡破裂。除神经内分泌因素外,我们认为肝脏向垂体传递的瘦素信号减少可能是对GH过表达及由此导致的青春期启动延迟的一种反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/f0c4222ac13d/fendo-09-00131-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/d02edd12780f/fendo-09-00131-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/2266d6c5e4b7/fendo-09-00131-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/4cca2508889b/fendo-09-00131-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/e9427b938b44/fendo-09-00131-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/a904d9773510/fendo-09-00131-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/57a7a280ec77/fendo-09-00131-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/f0c4222ac13d/fendo-09-00131-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/d02edd12780f/fendo-09-00131-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/2266d6c5e4b7/fendo-09-00131-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/4cca2508889b/fendo-09-00131-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/e9427b938b44/fendo-09-00131-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/a904d9773510/fendo-09-00131-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/57a7a280ec77/fendo-09-00131-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e4/5880896/f0c4222ac13d/fendo-09-00131-g007.jpg

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