咖啡馆饮食诱导的肥胖症恶化了实验性CKD
Jonas Laget1, Irene Cortijo1, Juliana H Boukhaled1
1RD-Néphrologie, 34090 Montpellier, France.
Nutrients
|August 12, 2023
概括
肥胖会加剧慢性病 (CKD) 的进展. 以前存在的肥胖症在小鼠5/6腎切除術后加重腎炎症和纖維症,具有高原和巨細胞標記物.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 代谢疾病研究研究
- 病理学 病理学 病理学
背景情况:
- 肥胖是慢性病 (CKD) 的一个主要风险因素.
- 了解肥胖如何影响CKD进展对于开发向疗法至关重要.
研究的目的:
- 在大鼠模型中研究肥胖对纤维化发展的影响.
- 分析在接受切除术的肥胖大鼠中特定纤维瘤标记物和炎症细胞的表达.
主要方法:
- 利用5/6切除术 (SNx) 和食堂饮食诱导肥胖的老鼠模型.
- 量化了原蛋白类型 (1, 3, 4),脂肪细胞大小,巨细胞透,以及脏和外皮皮质白脂肪组织 (eWAT) 中的阿迪波金水平.
主要成果:
- 与对照组相比,肥胖大鼠 (Cafeteria-SNx) 的脏原蛋白3和4表达显著增加.
- 在Cafeteria-SNx组中观察到细胞透的显著增加.
- 在肥胖的,腎切除的老鼠中,發現了高水平的特定阿迪波金,包括INTERLEUKIN 11 (IL11),二二基化酶4 (DPP4) 和素1 .
结论:
- 以前存在的肥胖会加剧CKD诱导的炎和纤维化.
- IL11,DPP4和serpin1可能在促进肥胖个体纤维化和恶化病方面发挥直接作用.
- 向这些阿迪波金可以为肥胖患者的CKD管理提供治疗策略.
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