肥胖脂肪细胞已经改变了降氧平衡与代谢后果
1Scientific Director Centre of Obesity, Marche Polytechnic University, Via Tronto 10a, 60126 Ancona, Italy.
Antioxidants (Basel, Switzerland)
|July 29, 2023
概括
肥胖会导致白色脂肪细胞内质网膜压力,导致炎症,胰岛素抵抗和2型糖尿病. 白色到棕色的脂肪组织转差为代谢障碍提供了新的治疗策略.
科学领域:
- 脂肪组织生物学 脂肪组织生物学
- 代谢障碍 代谢障碍 代谢障碍
- 细胞应激反应的细胞应激反应
背景情况:
- 白色和棕色的脂肪组织形成一个器官,肥胖的脂肪细胞表现出过度缩和内质网膜应激.
- 这种由活性氧物种驱动的压力激活了NLRP3炎症体,导致脂肪细胞死亡和碎片.
- 巨细胞清理碎片导致胰岛素抵抗和β细胞功能障碍,导致2型糖尿病.
研究的目的:
- 研究将脂肪细胞功能障碍与代谢疾病联系在一起的机制.
- 探索细胞内膜网膜应激和炎症酶激活在肥胖中的作用.
- 评估脂肪组织转分化的治疗潜力.
主要方法:
- 对脂肪细胞有机体变化的分析和内质网膜压力标志物的分析.
- 对反应性氧物种,NLRP3炎症体和火灭亡途径的研究.
- 评估巨细胞活动和分泌产物.
- 评估胰岛素受体信号传递和胰腺β细胞功能.
- 在小鼠和人类中研究白色到棕色脂肪组织的转差.
主要成果:
- 肥胖引起的内质网膜压力促进了NLRP3炎症酶激活和脂肪细胞烧灭.
- 巨细胞衍生因素干扰胰岛素受体活性,导致胰岛素抵抗.
- 脂肪细胞死亡和炎症有助于β细胞脱差和2型糖尿病.
- 白色到棕色的脂肪组织转差是哺乳动物中验证的现象.
结论:
- 脂肪组织功能障碍,以细胞应激和炎症为特征,驱动代谢疾病的进展.
- 准内等质网膜应激和炎症酶通路可能会减轻与肥胖有关的并发症.
- 白色到棕色的脂肪组织转差表现为肥胖和相关疾病的有希望的治疗途径.
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