Obesity and kidney disease: differential effects of obesity on adipose tissue and kidney inflammation and fibrosis.
Obesity and kidney disease: differential effects of obesity on adipose tissue and kidney inflammation and fibrosis.
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DOI：
10.1097/mnh.0000000000000087
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发表时间：
2015-01
影响因子：
3.2
通讯作者：
Sharma K
中科院分区：
文献类型：
--
作者：
Declèves AE;Sharma K
这篇综述通过研究肥胖期间脂肪组织和肾脏之间的潜在串扰提供了一个视角。众所周知，过多的卡路里摄入会导致器官损伤。相关的肥胖症增加会引发一系列细胞事件，导致进行性肥胖相关疾病，如肾脏疾病。最近的证据表明，脂肪组织产生的生物活性物质有助于肥胖相关的肾脏疾病，改变肾脏的功能和结构。同时，在肥胖状态下，脂肪组织内的促炎过程也会导致肾脏的病理生理变化。尽管在更好地描述肥胖相关代谢性疾病的病理生理学方面做出了相当大的努力，但仍然缺乏有效的治疗策略。新的策略侧重于调节脂肪功能，包括AMP激活的蛋白激酶激活、NADPH氧化酶功能和转化生长因子-b，这可能有助于减轻脂肪炎症，也可能提供肾脏保护。
This review provide a perspective by investigating the potential cross-talk between the adipose tissue and the kidney during obesity. It is well established that excessive caloric intake contributes to organ injury. The associated increased adiposity initiates a cascade of cellular events that leads to progressive obesity-associated diseases such as kidney disease. Recent evidence has indicated that adipose tissue produces bioactive substances that contribute to obesity-related kidney disease, altering the renal function and structure. In parallel, proinflammatory processes within the adipose tissue can also lead to pathophysiological changes in the kidney during the obese state. Despite considerable efforts to better characterize the pathophysiology of obesity-related metabolic disease, there are still a lack of efficient therapeutic strategies. New strategies focused on regulating adipose function with respect to AMP-activated protein kinase activation, NADPH oxidase function, and TGF-b may contribute to reducing adipose inflammation that may also provide renoprotection.