15-Deoxy-delta 12,14-prostaglandin J2 是脂肪细胞决定因子 PPAR 玛的配体
B M Forman1, P Tontonoz, J Chen
1Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Cell
|December 1, 1995
概括
研究人员确定了15-deoxy-delta 12,14-prostaglandin J2作为脂肪生成的关键调节剂,同时作为PPAR玛配体和脂肪细胞发育的诱导剂. 这一发现突出了代谢健康的关键途径.
科学领域:
- 分子内分泌学分子内分泌学
- 细胞生物学 细胞生物学
- 代谢调节 代谢调节 代谢调节
背景情况:
- 脂肪细胞质量调节对于脊椎动物的平衡至关重要.
- 纤维细胞转化为脂肪细胞是由氧酶增殖器激活受体玛 (PPARγ) 表达的介导.
- 内生PPARγ配体的存在表明它在调节脂肪生成方面发挥了作用.
研究的目的:
- 为了识别激活PPAR反应元素的内源配体.
- 为了研究这些配体在脂肪生成中的作用.
- 探索涉及PPARγ在脂肪细胞发育和葡萄糖平衡中的信号通路.
主要方法:
- 对PPAR反应元件激活的阿拉基多酸代谢物的查.
- 评估已识别的化合物的诱导脂肪生成的能力.
- 研究 thiazolidinedione 药物与 PPARγ 的结合.
主要成果:
- 15-deoxy-delta12,14-prostaglandin J2被确定为PPARγ配体和脂肪生成的诱导剂.
- thiazolidinedione 抗糖尿病药物也与 PPARγ 结合,并调节脂肪细胞的发育.
- 前列腺素和 thiazolidinedione 都使用一个共同的 PPARγ 信号通路.
结论:
- PPARγ及其内源配体在脂肪细胞发育和葡萄糖平衡中发挥着关键作用.
- PPARγ信号通路是代谢障碍干预的关键目标.
- 这项研究阐明了代谢调节的一个基本机制.
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