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Adipocytes and macrophages: Two engines powering inflammation in obesity and its complications

机译:脂肪细胞和巨噬细胞:两种驱动肥胖症及其并发症发炎的引擎

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摘要

Up to the discovery of leptin in 1994, white adipose tissue (WAT) was considered only an energy storage organ. However, in the last years, several proteic factors have been isolated from WAT revealing intriguing endocrine/paracrine/autocrine activities, i.e., WAT is involved in appetite modulation, immunity, reproductive system, bone metabolism, inflammation and energy expenditure. Obesity is characterized by a low chronic inflammatory state that contributed to the deleterious consequences of this pandemic disease that arise from several factors, including over-production of inflammatory mediators, hypoxia and macrophage infiltration. To note, low chronic inflammation state and hypoxia in obese subjects might be the major contributors for macrophage infiltration in adipose tissue. Noteworthy, it is an active crosstalk between adipocytes, pre-adipocytes and macrophages which results in a perpetuation of pro-inflammatory response. In line with this, pro-inflammatory cytokines and macrophages can be considered relevant factors involved in obesity-related disorders such as insulin insensitivity, type 2 diabetes and atherosclerosis. This short review will summarize some of the recent studies that have advanced our understanding of the main mechanisms that are at play in many serious, obesity-related comorbid diseases: systemic inflammation initiated in white adipose tissue and macrophages invasion and activation.
机译:直到1994年瘦素的发现,白色脂肪组织(WAT)才被认为只是一种能量储存器官。然而,在最近几年中,从WAT中分离出几种蛋白质因素,显示出令人感兴趣的内分泌/旁分泌/自分泌活性,即,WAT涉及食欲调节,免疫,生殖系统,骨代谢,炎症和能量消耗。肥胖症的特征是慢性炎症状态低,导致这种大流行性疾病的有害后果,这是由多种因素引起的,包括炎症介质的过度产生,缺氧和巨噬细胞浸润。要注意的是,肥胖者的低慢性炎症状态和缺氧可能是脂肪组织中巨噬细胞浸润的主要因素。值得注意的是,这是脂肪细胞,前脂肪细胞和巨噬细胞之间的活跃串扰,导致持续的促炎反应。与此相一致,促炎细胞因子和巨噬细胞可以被认为是与肥胖相关的疾病(如胰岛素敏感性低下,2型糖尿病和动脉粥样硬化)的相关因素。这篇简短的综述将总结一些最近的研究,这些研究使我们进一步了解了许多严重的,与肥胖相关的合并症:主要由白色脂肪组织引起的全身性炎症以及巨噬细胞的侵袭和激活。

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