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脂肪三糖脂酶介导的脂肪细胞脂解加剧了小鼠模型和患者中的急性胰腺炎严重程度
Xiaochun Xie1, Yang Liu1, Qi Yang2
1Department of Critical Care Medicine, Nanjing Jinling Hospital, Medical School of Southeast University, Nanjing, China; Medical School of Southeast University, Nanjing, China.
在急性胰腺炎 (AP) 中,内脏脂肪分解的增加与更糟糕的结果相关. 脂肪三甘油脂酶 (ATGL) 驱动的脂解会恶化AP,这表明ATGL是潜在的治疗标.
科学领域:
- 代谢性疾病研究研究.
- 胃肠病学 胃肠病学
- 病理生理学 病理生理学
背景情况:
- 脂肪细胞中的脱脂溶解在疾病发病过程中至关重要.
- 脂肪三甘油脂酶 (ATGL) 是脂肪细胞脂解的关键.
- 在急性胰腺炎 (AP) 中,ATGL介导的脂解的作用尚不清楚.
研究的目的:
- 调查内脏脂肪组织消耗和AP预后之间的关联.
- 阐明ATGL介导的脂解在AP病变发生中的作用.
- 评估ATGL抑制作为AP的治疗策略.
主要方法:
- 在AP患者和小鼠模型中测量了内脏脂肪组织消耗.
- 在白素诱导的AP小鼠模型中评估脂解和ATGL表达.
- 使用脂解刺激剂,ATGL淘汰赛小鼠,以及ATGL抑制剂atglistatin.
主要成果:
- 在AP患者中,较高的内脏脂肪组织消耗与不良预后相关.
- 在AP小鼠中,脂解和ATGL表达升高,而脂解刺激加剧了AP.
- 脂肪组织特异性ATGL淘汰和atglistatin治疗改善了瘦身和肥胖小鼠的AP.
结论:
- 通过ATGL介导的脂肪细胞脂解会加剧急性胰腺炎.
- 针对ATGL提供了一个潜在的治疗策略来管理AP.
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