Baqué S, Roca A, Guinovart J J, Gómez-Foix A M
Department of Bioquímica i Biologia Molecular, Facultat de Química, Universitat de Barcelona, Spain.
Eur J Biochem. 1996 Mar 15;236(3):772-7. doi: 10.1111/j.1432-1033.1996.t01-1-00772.x.
The direct effects of dexamethasone on glycogen synthase and phosphorylase and glycogen content have been investigated in primary cultured rat hepatocytes. Dexamethasone induced the transient translocation of glycogen synthase from the soluble to the 10000xg pelletable fraction and the activation of this enzyme, although more significant, longer-standing activation was achieved in the pelletable fraction. Neither total glycogen synthase content nor glycogen synthase mRNA levels were modified. Dexamethasone also caused the sustained activation (up to 6h) of glycogen phosphorylase, which was not accompanied by an increase in its mRNA level. Glycogen cell content and the incorporation of (14C) glucose into glycogen decreased after dexamethasone treatment. The data show that dexamethasone, unlike other glycogenolytic hormones, at concentrations of 10 nM or higher, stimulate hepatocyte glycogenolysis without inducing the inverse coupling of synthase and phosphorylase. The co-existence of active forms of both glycogen synthase and phosphorylase promoted by dexamethasone leads to a situation that is analogous to that of the fasted liver.
在地鼠原代培养肝细胞中，研究了地塞米松对糖原合酶、磷酸化酶和糖原含量的直接影响。地塞米松可诱导糖原合酶从可溶性部分短暂转位至10000xg可沉淀部分，并激活该酶，尽管在可沉淀部分可实现更显著、更持久的激活。糖原合酶的总含量和糖原合酶mRNA水平均未改变。地塞米松还可导致糖原磷酸化酶的持续激活（长达6小时），但其mRNA水平并未升高。地塞米松处理后，糖原细胞含量以及（14C）葡萄糖掺入糖原的量均降低。数据表明，与其他糖原分解激素不同，浓度为10 nM或更高的地塞米松可刺激肝细胞糖原分解，而不会诱导合酶和磷酸化酶的反向偶联。地塞米松促进的糖原合酶和磷酸化酶活性形式的共存导致了一种类似于饥饿肝脏的情况。
