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Cell Metab:澳洲学者找到大脑控制脂肪燃烧开关

摘要 : 2017年8月1日,国际著名学术杂志《Cell》子刊《Cell metabolism》杂志在线发表了澳大利亚莫纳什大学Tony Tiganis研究员的一篇研究论文,研究报告了研究组找到控制脂肪燃烧的大脑开关,有望为治疗肥胖症带来新方法。

2017年8月1日,国际著名学术杂志《Cell》子刊《Cell metabolism》杂志在线发表了澳大利亚莫纳什大学Tony Tiganis研究员的一篇研究论文,研究报告了研究组找到控制脂肪燃烧的大脑开关,有望为治疗肥胖症带来新方法。

人体内的白色脂肪主要用于储能,而棕色脂肪则负责消耗能量,本次研究发现了白色脂肪转变为棕色脂肪的所谓脂肪棕化过程。研究表明,用餐之后,人体内的血糖浓度升高,胰岛素的分泌量增加,大脑随之发出信号,促进脂肪棕化,增加能量消耗;相反,不用餐时,大脑则指示棕色脂肪转变为白色脂肪,储存能量。

提贾尼斯说,为了保证体重不过多增加或过多减少,大脑中有一个类似开关的机制,在用餐时关闭以促进脂肪棕化,不用餐时则打开以抑制脂肪棕化。但在肥胖患者中,这个开关却始终打开,脂肪棕化一直受抑制。

提贾尼斯说,他们接下来计划探索通过控制这个开关,促进脂肪燃烧从而达到减肥的目的。但他同时强调,任何潜在减肥疗法都还有很长的路要走。

原文链接:

A Hypothalamic Phosphatase Switch Coordinates Energy Expenditure with Feeding

原文摘要:

Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure. The feeding-induced repression of hypothalamic TCPTP was defective in obesity. Mice lacking TCPTP in AgRP/NPY neurons were resistant to diet-induced obesity and had increased beige fat activity and energy expenditure. The deletion of hypothalamic TCPTP in obesity restored feeding-induced browning and increased energy expenditure to promote weight loss. Our studies define a hypothalamic switch that coordinates energy expenditure with feeding for the maintenance of energy balance.

来源: Cell metabolism 浏览次数:0

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