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多囊卵巢综合征肥胖女性黄素化颗粒细胞中瘦素长型受体mRNA的表达

Expression of leptin long-form receptor mRNA in luteinized granulosa cells of obese women with polycystic ovary syndrome.

作者信息

Yin Jie, Liu Yi, Lv Liqun, Wang Donghua, Gong Cheng, Xiao Wei, Sheng Hui

机构信息

Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2007 Aug;27(4):461-3. doi: 10.1007/s11596-007-0429-y.

DOI:10.1007/s11596-007-0429-y
PMID:17828512
Abstract

To investigate the expression of mRNA of leptin long-form receptor (OB-Rb) in luteinized granulosa cells of obese women with polycystic ovary syndrome (PCOS), and to determine the role of leptin in the physiopathology of PCOS, luteinized granulosa cells were collected from the follicle fluid of 10 obese women who met the diagnostic criteria for PCOS and their BMI was equal to or greater than 25 kg/m(2), and at the same time, granulosa cells were collected from 10 normal women undergoing IVF-ET who served as the control group. Some luteinized granulosa cells were taken from normal women for in-vitro culture, into which human leptin of different concentrations was added (0, 10, 100 and 1000 ng/mL). After stimulation with leptin for 48 h, RT-PCR was employed for the detection of the expression of OB-RLmRNA in the luteinized granulosa cells. Our results showed that the level of OB-RLmRNA in luteinized granulosa cells of obese PCOS women was higher than those in the control (P<0.05). In luteinized granulosa cells cultured in vitro and stimulated by human leptin for 48 h, the level of OB-RLmRNA was higher than those without leptin stimulation (P<0.01), and when leptin concentration was at 100 ng/mL, and the level of OB-R(L)mRNA reached a peak. It is concluded that in obese PCOS women, the level of serum leptin is increased, which promotes the expression of OB-R(L) in luteinized granulosa cells and increases the sensitivity of the granulosa cells to leptin. Leptin may contribute to anovulation in obese women with PCOS.

摘要

为研究多囊卵巢综合征(PCOS)肥胖女性黄素化颗粒细胞中瘦素长型受体(OB-Rb)mRNA的表达情况,并确定瘦素在PCOS病理生理过程中的作用,收集了10名符合PCOS诊断标准且体重指数(BMI)等于或大于25kg/m²的肥胖女性卵泡液中的黄素化颗粒细胞,同时收集了10名接受体外受精-胚胎移植(IVF-ET)的正常女性的颗粒细胞作为对照组。取部分正常女性的黄素化颗粒细胞进行体外培养,向其中加入不同浓度的人瘦素(0、10、100和1000ng/mL)。用瘦素刺激48小时后,采用逆转录聚合酶链反应(RT-PCR)检测黄素化颗粒细胞中OB-RLmRNA的表达。结果显示,肥胖PCOS女性黄素化颗粒细胞中OB-RLmRNA水平高于对照组(P<0.05)。在体外培养并用瘦素刺激48小时的黄素化颗粒细胞中,OB-RLmRNA水平高于未用瘦素刺激的细胞(P<0.01),当瘦素浓度为100ng/mL时,OB-R(L)mRNA水平达到峰值。结论是,肥胖PCOS女性血清瘦素水平升高,促进了黄素化颗粒细胞中OB-R(L)的表达,增加了颗粒细胞对瘦素的敏感性。瘦素可能导致肥胖PCOS女性排卵障碍。

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本文引用的文献

1
[Expression of leptin mRNA in luteinized granulosa cells and leptin levels in serum and follicular fluid of non-obese infertile patients with polycystic ovary syndrome].[非肥胖型多囊卵巢综合征不孕患者黄体化颗粒细胞中瘦素mRNA的表达及血清和卵泡液中瘦素水平]
Zhonghua Yi Xue Za Zhi. 2005 Jan 12;85(2):88-91.
2
Serum leptin elevation in obese women with PCOs: a continuing controversy.患有多囊卵巢综合征的肥胖女性血清瘦素升高:持续存在的争议。
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3
Serum leptin levels correlate with obesity parameters but not with hyperinsulinism in women with polycystic ovary syndrome.
多囊卵巢综合征女性的血清瘦素水平与肥胖参数相关,但与高胰岛素血症无关。
Fertil Steril. 2004 Nov;82(5):1364-8. doi: 10.1016/j.fertnstert.2004.04.049.
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Improving reproductive performance in overweight/obese women with effective weight management.通过有效的体重管理提高超重/肥胖女性的生殖能力。
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Leptin receptor variant in women with polycystic ovary syndrome.多囊卵巢综合征女性中的瘦素受体变体
Fertil Steril. 2002 Dec;78(6):1334-5. doi: 10.1016/s0015-0282(02)04352-2.
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Evidence of leptin expression in normal and polycystic human ovaries.瘦素在正常及多囊人卵巢中的表达证据。
Mol Hum Reprod. 2001 Dec;7(12):1143-9. doi: 10.1093/molehr/7.12.1143.
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Serum and follicular fluid leptin during in vitro fertilization: relationship among leptin increase, body fat mass, and reduced ovarian response.体外受精过程中的血清和卵泡液瘦素:瘦素增加、体脂量与卵巢反应降低之间的关系。
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Suppression of leptin during lactation: contribution of the suckling stimulus versus milk production.哺乳期瘦素的抑制:哺乳刺激与乳汁分泌的作用
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Leptin antagonizes the insulin-like growth factor-I augmentation of steroidogenesis in granulosa and theca cells of the human ovary.瘦素拮抗胰岛素样生长因子-I对人卵巢颗粒细胞和卵泡膜细胞类固醇生成的增强作用。
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