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中部肥胖是否反映了"预兆的库辛病"?
I J Bujalska1, S Kumar, P M Stewart
1Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, UK.
Lancet (London, England)
|April 26, 1997
概括
中部肥胖与代谢问题有关. 与皮下脂肪细胞不同,体脂肪细胞可以通过11β-基类固醇脱酶1 (11β-HSD1) 将非活性皮质转化为活性皮质醇,这可能解释了肥胖症.
科学领域:
- 内分泌学 在内分泌学.
- 代谢综合征是代谢综合征的一种.
- 脂肪组织生物学 脂肪组织生物学
背景情况:
- 中心肥胖与代谢功能障碍和死亡率增加有关.
- 葡萄皮质皮质醇和皮质醇一样,在脂肪组织调节中起着关键作用,当过量时,可以导致中心肥胖.
- 酶11β-基类固醇脱酶 (11β-HSD) 通过与非活性皮质醇相互转换来调节活性皮质醇水平.
研究的目的:
- 为了研究不同脂肪组织储存区内的皮质醇代谢.
- 分析11种β-HSD异型体在人体体内和皮下脂肪 stromal 细胞中的表达和活性.
主要方法:
- 从16名接受选择性腹部手术的患者获得了培养的体和皮下脂肪 stromal 细胞.
- 在这些细胞培养物中分析了11种β-HSD异型 (1和2) 的表达和活性.
- 用皮质醇和胰岛素对细胞进行治疗,以评估对酶活性的影响.
主要成果:
- 只有11β-HSD1异型在脂肪 stromal 细胞表达.
- 11β-HSD1表现出主要的氧降解酶活性 (皮质醇转化为皮质醇转化),在体内脂肪中明显高于皮下脂肪.
- 用皮质醇和胰岛素治疗的口腔脂肪 stromal 细胞显示,11β-HSD1 oxo-reductase 活性进一步增加.
结论:
- 来自体脂肪的脂肪性 stromal 细胞具有通过11β-HSD1从皮质素产生活性皮质醇的能力,这种功能在皮下脂肪中没有观察到.
- 由于暴露于皮质醇和胰岛素,体脂肪中的皮质醇生成能力得到增强.
- 这些发现表明,体脂肪组织中的局部机制可能导致中心肥胖,可能模仿局部形式的库辛综合征.
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