p-Synephrine stimulates glucose consumption via AMPK in L6 skeletal muscle cells
- 作者：Na-Young Hong ; Zhi-Gang Cui ; Hee-Kyoung Kang ; Dae-Ho Lee ; Young-Ki Lee ; Deok-Bae Park ; parkdb@jejunu.ac.kr
- 关键词：p-Synephrine ; Glucose consumption ; Glut4 ; AMPK
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2012
- 期刊代码：159_0006291x
- 类别：bio
- 出版时间：24 February, 2012
- 卷：418
- 期：4
- 页码：720-724
- 文件大小：439 K
摘要
Interest in p-synephrine, the primary protoalkaloid in the extract of bitter orange and other citrus species, has increased due to its various pharmacological effects and related adverse effects. The lipolytic activity of p-synephrine has been repeatedly revealed by in vitro and in vivo studies and p-synephrine is currently marketed as a dietary supplement for weight loss. The present study investigated the effect of p-synephrine on glucose consumption and its action mechanism in L6 skeletal muscle cells. Treatment of L6 skeletal muscle cells with p-synephrine (0-100 渭M) did not affect cell viability and increased basal glucose consumption up to 50%over the control in a dose-dependent manner. The basal- or insulin-stimulated lactic acid production as well as glucose consumption was significantly increased by the addition of p-synephrine. p-Synephrine stimulated the phosphorylation of AMPK but not of Akt. p-Synephrine-induced glucose consumption was sensitive to the inhibition of AMPK but not to the inhibition of PI3 kinase. p-Synephrine also stimulated the translocation of Glut4 from the cytoplasm to the plasma membrane; this stimulation was suppressed by the inhibition of AMPK, but not of PI3 kinase. Taken together, p-synephrine can stimulate glucose consumption (Glut4-dependent glucose uptake) by stimulating AMPK activity, regardless of insulin-stimulated PI3 kinase-Akt activity in L6 skeletal muscle cells.