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首页> 外文期刊>Journal of Cellular Physiology >Adipocytes properties and crosstalk with immune system in obesity‐related inflammation
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Adipocytes properties and crosstalk with immune system in obesity‐related inflammation

机译:脂肪细胞与免疫属性和相声系统在肥胖相关的炎症

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Obesity is a condition likely associated with several dysmetabolic conditions or worsening of cardiovascular and other chronic disturbances. A key role in this mechanism seem to be played by the onset of low‐grade systemic inflammation, highlighting the importance of the interplay between adipocytes and immune system cells. Adipocytes express a complex and highly adaptive biological profile being capable to selectively activate different metabolic pathways in order to respond to environmental stimuli. It has been demonstrated how adipocytes, under appropriate stimulation, can easily differentiate and de‐differentiate thereby converting themselves into different phenotypes according to metabolic necessities. Although underlying mechanisms are not fully understood, growing in adipocyte size and the inability of storing triglycerides under overfeeding conditions seem to be crucial for the switching to a dysfunctional metabolic profile, which is characterized by inflammatory and apoptotic pathways activation, and by the shifting to pro‐inflammatory adipokines secretion. In obesity, changes in adipokines secretion along with adipocyte deregulation and fatty acids release into circulation contribute to maintain immune cells activation as well as their infiltration into regulatory organs. Over the well‐established role of macrophages, recent findings suggest the involvement of new classes of immune cells such as T regulatory lymphocytes and neutrophils in the development inflammation and multi systemic worsening. Deeply understanding the pathways of adipocyte regulation and the de‐differentiation process could be extremely useful for developing novel strategies aimed at curbing obesity‐related inflammation and related metabolic disorders.
机译:肥胖是一个条件可能相关几个dysmetabolic条件或恶化心血管疾病和其他慢性障碍。关键似乎在该机制中所扮演的角色低优先级的爆发系统性炎症,强调相互作用的重要性脂肪细胞和免疫系统细胞之间。脂肪细胞表达一个复杂和高度适应性生物文件能够选择性地激活不同的代谢途径,以对环境的刺激作出反应。演示了如何脂肪细胞,在适当的刺激,很容易区分de分化从而把自己根据代谢成不同的表型生活必需品。没有完全理解,在脂肪细胞的大小无法将储存的甘油三酯喂食过多的条件似乎是至关重要的切换到不正常的新陈代谢,特点是炎症和凋亡通路的激活,转向支持炎症发病分泌。分泌脂肪细胞放松管制和脂肪酸释放进入循环的贡献维持免疫细胞的激活以及他们渗透到监管机构。最近好检测巨噬细胞的作用,建立结果表明新类的参与T调节淋巴细胞等免疫细胞和中性粒细胞炎症发展和多系统的恶化。了解脂肪细胞的途径监管和德检测分化过程可能是非常有用的对于发展中小说策略旨在遏制肥胖相关炎症和代谢紊乱有关。

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