Background Obesity is a risk factor for chronic kidney disease (CKD). While the exact mechanisms remain unclear, inflammation may be a consequence of obesity that directly impacts the kidneys. The aim of this study was to examine the inflammatory status of the kidneys and potential ongoing renal damage, i.e., tubular damage and fibrosis after long-term obesity maintained through persistent consumption of a high-fat diet (HFD). Results Twenty-four-week-old male Long-Evans (LEV) rats were continuously fed a control diet (CD) or HFD for 51 weeks. The mean body weight was higher in HFD-fed rats than in control diet-fed rats and markedly elevated during the last 24 weeks. Blood analyses revealed no substantial alterations in renal functional parameters by HFD consumption but a substantial increase in creatine kinase, a muscle loss marker. Magnetic resonance imaging (MRI) was utilized to quantify rat quadriceps muscle mass. The data showed that HFD-induced obesity in LEV rats was accompanied by minor decreases in muscle mass and strength at 75 weeks of age. Rat kidney inflammatory status was evaluated using histological and immunohistological techniques. The number of foci with immune cell infiltrates and infiltrating monocytes/macrophages was significantly increased in HFD-fed rat kidneys at week 75. Renal fibrosis parameters, including glomerulosclerosis and tubular damage, were also markedly increased in renal tissues from HFD-fed rats compared to the controls. The significant increase in tubular protein casts in HFD-fed rat tissues indicated that renal function was already disturbed. Rat kidney inflammatory status was further evaluated using the simultaneous profiling of twenty-two inflammatory markers in kidney tissue extracts. Consistently, MCP-1 and eotaxin (CCL11) levels were elevated in obese LEV rat kidneys. Conclusions Compared to CD-fed rats, HFD-fed obese LEV rats show significant damage of renal structures with aging. These subtle changes may sensitize the kidneys to the development of progressive CKD.

中文翻译：

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高脂饮食诱导的肥胖会在衰老的 Long-Evans 大鼠的肾脏中引起炎症微环境。

背景 肥胖是慢性肾脏病 (CKD) 的危险因素。虽然确切的机制仍不清楚，但炎症可能是肥胖直接影响肾脏的结果。本研究的目的是检查肾脏的炎症状态和潜在的持续性肾损伤，即通过持续食用高脂肪饮食 (HFD) 维持长期肥胖后的肾小管损伤和纤维化。结果 24 周龄雄性 Long-Evans (LEV) 大鼠连续喂食对照饮食 (CD) 或 HFD 51 周。HFD 喂养大鼠的平均体重高于对照组饮食喂养的大鼠，并且在过去 24 周内显着升高。血液分析显示，HFD 消耗不会显着改变肾功能参数，但肌酸激酶（肌肉损失标志物）显着增加。磁共振成像 (MRI) 用于量化大鼠股四头肌肌肉质量。数据显示，在 LEV 大鼠中，HFD 引起的肥胖伴随着 75 周龄时肌肉质量和力量的轻微下降。使用组织学和免疫组织学技术评估大鼠肾脏炎症状态。在第 75 周，HFD 喂养的大鼠肾脏中具有免疫细胞浸润和浸润单核细胞/巨噬细胞的病灶数量显着增加。与 HFD 喂养大鼠的肾组织相比，肾纤维化参数，包括肾小球硬化和肾小管损伤也显着增加控件。HFD 喂养的大鼠组织中肾小管蛋白管型的显着增加表明肾功能已经受到干扰。使用同时分析肾组织提取物中的 22 种炎症标志物进一步评估大鼠肾脏炎症状态。一致地，MCP-1 和 eotaxin (CCL11) 水平在肥胖 LEV 大鼠肾脏中升高。结论 与 CD 喂养的大鼠相比，HFD 喂养的肥胖 LEV 大鼠肾脏结构随着年龄的增长而出现明显的损害。这些细微的变化可能会使肾脏对进行性 CKD 的发展敏感。