Adipocyte cell death, fatty liver disease and associated metabolic disorders.
Adipocyte cell death, fatty liver disease and associated metabolic disorders.
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脂肪细胞细胞死亡，脂肪肝病和相关的代谢疾病。
DOI：
10.1159/000360509
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Feldstein AE
中科院分区：
文献类型：
--
作者：
Eguchi A;Feldstein AE
在美国和世界许多其他地区，肥胖已达到流行病的程度。肥胖会增加多种不良健康状况的风险，包括 2 型糖尿病、胰岛素抵抗、血脂异常、高血压和肝脂肪变性。脂肪细胞肥大发生在体重增加期间，并且与免疫细胞（主要是巨噬细胞）招募到脂肪组织（AT）有关。这些细胞通常围绕着垂死或死亡的脂肪细胞，形成冠状结构，这种结构存在于肥胖实验模型以及肥胖人类中。 AT 的免疫浸润导致各种脂肪因子、细胞因子和趋化因子的产生增加，这些因子在胰岛素抵抗和肝脂肪变性的发展中发挥着至关重要的作用。导致 AT 巨噬细胞募集的致病机制正在深入研究中，但仍不完全清楚。最近的证据表明，在应激肥大的脂肪细胞中，各种程序性细胞死亡途径被激活，并可能导致细胞死亡。这些事件似乎发生在早期阶段，并且对于引发与肥胖相关的代谢失调非常重要。
Obesity has reached epidemic proportions in the US and many other parts of the world. Obesity increases the risk of a number of adverse health conditions including type 2 diabetes, insulin resistance, dyslipidemia, hypertension, and hepatic steatosis. Adipocyte hypertrophy occurs during weight gain and is associated with recruitment of immune cells mainly macrophages into the adipose tissue (AT). These cells typically surround a dying or dead adipocyte with the formation of crown-like structures that are present in experimental models of obesity as well as obese humans. The immune infiltration of AT results in increased production of various adipokines, cytokines, and chemokines that play a crucial role in the development of insulin resistance and hepatic steatosis. The pathogenic mechanisms resulting in AT macrophage recruitment are under intense investigation and remain incompletely understood. Recent evidence suggests that various programmed cell death pathways are activated in stressed hypertrophied adipocytes and may result in cell death. These events appear to occur at early stages and be important in triggering the metabolic dysregulation associated with obesity.