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通过饮食中的蛋白质负载加速的囊生成取决于,但不是由脏巨细胞启动的

Randee Sedaka¹, Jifeng Huang¹, Shinobu Yamaguchi¹

¹Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.

Frontiers in medicine

|August 4, 2023

概括

高蛋白饮食通过增加脏对上皮细胞的谷氨酸输送来加速小鼠自身主导性多囊性病 (ADPKD) 的进展,促进炎症前早期囊生长. 长期高蛋白饮食也增加了巨细胞的激活,恶化了细胞生成.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
饮食科学饮食科学

背景情况:

自体主导多囊性病 (ADPKD) 的严重程度受饮食因素的影响.
饮食中摄入的蛋白质可以通过脏缩和炎症加速ADPKD中的囊生长.
来自蛋白质代谢的特定氨基酸可能会刺激脏巨细胞,促进囊的进展.

研究的目的:

研究高蛋白 (HP) 饮食在ADPKD中促进囊发生的机制.
确定特定氨基酸和巨细胞激活在饮食诱导的囊生长中的作用.
为了区分早期与慢性高蛋白饮食暴露的影响.

主要方法:

在Pkd1KO小鼠中诱导的多囊性病 (PKD) 使用泰莫西芬.
养Pkd1KO小鼠的低 (LP),正常 (NP) 或高 (HP) 蛋白质饮食用于早期 (1周) 或慢性 (6周) 暴露.
分析脏组织组织学,免疫光,巨细胞标记物,并对管状上皮细胞进行RNA测序.

主要成果:

慢性HP饮食增加了Pkd1KO小鼠的脏重量,巨细胞透,炎症和囊指数.
大细胞枯竭减弱慢性HP饮食诱导的囊生长.
早期的HP饮食增加了脏大小和Snat3,Clcnka和Pepck1在管状细胞中的表达,与谷氨胺代谢和氨分泌有关.
早期的谷氨酸补充剂在Pkd1KO小鼠中诱导脏缩.

结论:

在Pkd1KO小鼠中,慢性高蛋白饮食诱导的病依赖于巨细胞的招募和炎症.
在高蛋白饮食下,囊的早期扩张是由增加对细胞的谷氨胺输送所驱动的,这在炎症之前发生.
针对氨基酸代谢的饮食干预可能为ADPKD提供新的治疗策略.

关键词:

谷氨胺是一种胺.高蛋白质的高蛋白质的高蛋白质.巨细胞是一个巨细胞.多囊性脏疾病多囊性脏疾病脏过高症脏过高症

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