Young M E, Radda G K, Leighton B
Department of Biochemistry, University of Oxford, U.K.
FEBS Lett. 1996 Mar 11;382(1-2):43-7. doi: 10.1016/0014-5793(96)00129-9.
We determined whether the cell permeable molecule AICAR, whose metabolite activates AMP-activated protein kinase (AMPK) in cells, affected glycogen metabolism in rat soleus muscle preparations in vitro. The basal and insulin-stimulated rates of radiochemical lactate formation, net lactate release and glycogen synthesis were determined. AICAR stimulated net lactate release (but not radiochemical lactate formation) only at a basal concentration of insulin. An increased rate of glycogenolysis was the likely cause of increased net lactate release as glycogen phosphorylase activity was significantly increased by AICAR. AICAR-stimulated net lactate release and phosphorylase activity were potently inhibited by insulin.
我们研究了细胞可渗透分子AICAR（其代谢产物可在细胞内激活AMP活化蛋白激酶（AMPK））是否会影响体外培养的大鼠比目鱼肌制剂中的糖原代谢。我们测定了基础状态和胰岛素刺激状态下放射性化学乳酸生成、净乳酸释放及糖原合成的速率。AICAR仅在基础胰岛素浓度下刺激净乳酸释放（而非放射性化学乳酸生成）。糖原分解速率增加可能是净乳酸释放增加的原因，因为AICAR可显著增加糖原磷酸化酶活性。胰岛素可有效抑制AICAR刺激的净乳酸释放及磷酸化酶活性。
