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机体应激或能干扰脂肪细胞的分化过程

来源:生物谷 2014-07-18 09:05

2014年7月18日讯 /生物谷BIOON/--近日,波士顿大学医学院(BUSM)研究人员使用实验模型,首次表明当人体处于应激环境下或炎症反应过程中所释放的代谢产物腺苷,能停止脂肪细胞分化过程(即脂肪干细胞分化成脂肪细胞)。

早期研究已经表明脂肪细胞分化过程通过调控细胞内脂肪的储存,使血液中不会累积高水平的脂肪,在保持健康的脂肪稳态中发挥核心作用。目前一项新的研究结果表明,人体应激反应有可能会阻断脂肪细胞的发育。

新研究发现脂肪细胞的发育过程被由腺苷受体--A2b腺苷受体(A2bAR)发送出的信号分子即KLF4所终止。随着A2bAR的表达,KLF4水平增高,从而抑制脂肪干细胞的分化。A2bAR和KLF4两因素之间的相关性导致脂肪细胞发育的中断,而这会导致细胞内脂肪的储存,以及脂肪进入血液过程出现问题。

虽然大多数的研究是在实验模型中完成的,但该小组还发现在人原发性前脂肪细胞培养系统中,A2bAR的激活能抑制脂肪形成。最后,分析肥胖者的脂肪组织后,发现皮下脂肪和内脏脂肪中A2bAR和KLF4表达之间有很强的关联。

新的研究表明,应激或炎症可以破坏脂肪组织的发育过程,这可能对脂肪细胞动态平衡过程产生负面影响。(生物谷Bioon.com)

详细英文报导:

Obesity may be impacted by stress, study says

Using experimental models, researchers at Boston University School of Medicine (BUSM) showed that adenosine, a metabolite released when the body is under stress or during an inflammatory response, stops the process of adipogenesis, when adipose (fat) stem cells differentiate into adult fat cells.

Previous studies have indicated adipogenesis plays a central role in maintaining healthy fat homeostasis by properly storing fat within cells so that it does not accumulate at high levels in the bloodstream. The current findings indicate that the body's response to stress, potentially stopping the production of fat cell development, might be doing more harm than good under conditions of obesity and/or high levels of circulating blood fat.

The process is halted due to a newly identified signaling from an adenosine receptor, the A2b adenosine receptor (A2bAR) to a stem cell factor, known as KLF4, which regulates stem cell maintenance. When A2bAR is expressed, KLF4 level is augmented, leading to inhibition of differentiation of fat stem cells. The correlation between these two factors leads to an interruption of fat cell development, which could result in issues with fat storage within the cells and it getting into the bloodstream.

While the majority of the study was carried out in experimental models, the group also showed that A2bAR activation inhibits adipogenesis in a human primary preadipocyte culture system. Finally, analysis of adipose tissue of obese subjects showed a strong association between A2bAR and KLF4 expression in both subcutaneous (under the skin) and visceral (internal organ) human fat.

"It may seem counterintuitive, but our body needs fat tissue in order to function properly, and certain biochemical cellular processes are necessary for this to happen," said Katya Ravid, DSc/PhD, professor of medicine and biochemistry at BUSM and director of the Evans Center for Interdisciplinary Biomedical Research who led the study. "Our study indicates that a dysfunction resulting from stress or inflammation can disrupt the process of fat tissue development, which could have a negative impact on processes dependent on proper fat cell homeostasis."

This study is part of ongoing research interest and investigations by researchers in Ravid's lab examining the differentiation of bone marrow and tissue stem cells and the role of adenosine receptors in this process.

 

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