James A P, Flynn C B, Jones S L, Palmer T N, Fournier P A
Department of Biochemistry, University of Western Australia, Nedlands, Western Australia 6907, Australia.
Biochem J. 1998 Jan 15;329 ( Pt 2)(Pt 2):341-7. doi: 10.1042/bj3290341.
The starved-to-fed transition is accompanied by rapid glycogen deposition in skeletal muscles. On the basis of recent findings [Bräu, Ferreira, Nikolovski, Raja, Palmer and Fournier (1997) Biochem. J. 322, 303-308] that during recovery from exercise there is a shift from a glucose 6-phosphate/phosphorylation-based control of glycogen synthesis to a phosphorylation-based control alone, this paper seeks to establish whether a similar shift occurs in muscle during re-feeding after starvation in the rat. Chow re-feeding after 48 h of starvation resulted in glycogen deposition in all muscles examined (white, red and mixed quadriceps, soleus and diaphragm) to levels higher than those in the fed state. Although the early phase of re-feeding was associated with increases in glucose 6-phosphate levels in all muscles, there was no accompanying increase in the fractional velocity of glycogen synthase except in the white quadriceps muscle. This finding, together with the observation that the fractional velocity of glycogen synthase in most muscles was already high in the starved state, suggests that in the initial phase of glycogen deposition the phosphorylation state of the enzyme may be adequate to support net glycogen synthesis. In the later phase of re-feeding, the progressive decrease in the fractional velocity of glycogen synthase in association with a decrease in the rate of glycogen deposition suggests that glycogen synthesis is controlled primarily by changes in the phosphorylation state of glycogen synthase. In conclusion, this study suggests that there is a temporal shift in the site of control of glycogen synthesis as glycogen deposition progresses during re-feeding after starvation.
从饥饿到进食的转变伴随着骨骼肌中糖原的快速沉积。基于最近的研究发现[布劳、费雷拉、尼科洛夫斯基、拉贾、帕尔默和富尔尼耶(1997年)《生物化学杂志》322卷,303 - 308页],即在运动恢复过程中,糖原合成的控制从基于6 - 磷酸葡萄糖/磷酸化的控制转变为仅基于磷酸化的控制,本文旨在确定在大鼠饥饿后重新进食期间,肌肉中是否会发生类似的转变。饥饿48小时后重新喂食普通饲料,导致所有检测的肌肉(白色、红色和混合股四头肌、比目鱼肌和膈肌)中的糖原沉积水平高于进食状态。尽管重新喂食的早期阶段与所有肌肉中6 - 磷酸葡萄糖水平的升高有关,但除了白色股四头肌外,糖原合酶的分数速度并没有随之增加。这一发现,连同在饥饿状态下大多数肌肉中糖原合酶的分数速度已经很高的观察结果,表明在糖原沉积的初始阶段,该酶的磷酸化状态可能足以支持糖原的净合成。在重新喂食的后期阶段,糖原合酶分数速度的逐渐下降与糖原沉积速率的下降相关,这表明糖原合成主要受糖原合酶磷酸化状态变化的控制。总之,这项研究表明,在饥饿后重新喂食期间,随着糖原沉积的进行,糖原合成控制位点存在时间上的转变。