氨酸B1受体缺乏会促进脂肪组织对β3-上腺刺激的热生成反应的增强
Jéssica Branquinho1, Raquel L Neves1, Renan P Martin1,2
1Center for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
概括
缺乏基宁B1受体 (B1R) 的小鼠显示能量消耗增加,脂肪组织热生成增强. 这表明B1R抗剂可能是肥胖和代谢障碍的治疗点.
科学领域:
- 脂肪组织生物学 脂肪组织生物学
- 代谢调节 代谢调节 代谢调节
- 热生成是一种热生成.
背景情况:
- 基宁B1受体 (B1R) 在脂肪细胞中起着至关重要的作用,影响肥胖和葡萄糖代谢.
- B1R是调节能量代谢和脂肪组织热生成的潜在治疗标.
研究的目的:
- 研究基因B1受体 (B1R) 在脂肪组织热生成和能量代谢中的作用.
- 评估B1R缺乏对冷暴露和药物刺激的代谢反应的影响.
主要方法:
- 使用了基宁B1淘汰赛 (B1KO) 的小鼠.
- 小鼠接受了CL 316,243的急性刺激和慢性感冒暴露.
- 在棕色和白色脂肪组织上进行了代谢,组织学,基因/蛋白质表达和RNA-seq分析.
主要成果:
- 在CL 316,243治疗后,B1KO小鼠在 inguinal 白脂肪组织 (iWAT) 中表现出增加的能量消耗和上调的热能基因.
- 在慢性感冒下,B1KO小鼠表现出增强的非发的热生成,增加间棕色脂肪组织 (iBAT) 质量 (~90%),并在iWAT中招募色脂肪细胞 (~50%).
- 观察到热源基因的显著上调 (例如,Ucp1,iWAT增加了14.5倍),以及胰岛素信号,氧化酸化和色通路的激活.
结论:
- 氨酸B1受体缺乏会改变脂肪组织的新陈代谢和基因表达,激活热生成途径并增加能量消耗.
- B1R对抗剂代表了管理肥胖和相关的代谢状况,如炎症和糖尿病的有前途的治疗策略.
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