Elucidation of the regulating mechanism of glycolipid synthesis by intracellular energy sensor AMPK

由于细胞糖基神经酰胺（glcer）的异常积累会引起戈谢病、帕金森病等多种疾病，因此需要将其量调节到适当的水平。然而，关于细胞如何调节glcer水平的见解尚不清楚。腺苷酸活化蛋白激酶（AMPK）是一种重要的细胞能量传感器，通过调节葡萄糖和脂质代谢来维持ATP水平。在本研究中，我们研究了AMPK是否影响GlcCer代谢，发现GlcCer的合成受到AMPK依赖机制的负调控。我们的研究结果表明，通过激活AMPK来降低glcer可能成为glcer积累引起的疾病的一种新的治疗选择。

The amount of cellular glucosylceramide (GlcCer) needs to be regulated in an appropriate level because the abnormal accumulation of GlcCer causes several diseases such as Gaucher's disease and Parkinson's disease. However, insights into how cells regulate GlcCer level are yet to be clarified. AMP-activated protein kinase (AMPK), which is a crucial cellular energy sensor, regulates glucose and lipid metabolism to maintain ATP level. In this study, we investigated whether AMPK affect GlcCer metabolism, and found that GlcCer synthesis was negatively regulated by AMPK-dependent mechanism. Our findings suggest that reduction of GlcCer by AMPK activation may become a new treatment option for diseases caused by the accumulation of GlcCer.