Liao T H, Szepesi B
J Nutr. 1980 Dec;110(12):2390-5. doi: 10.1093/jn/110.12.2390.
Liver glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40) activities were measured in rats that were starved for 2 days and then fed a high-glucose, adequate-protein diet for 3 days. During refeeding the rats were injected with thyroxine to block glycogen accumulations preceeding the enzyme "overshoot". The G6PD and ME "overshoot" at the end of refeeding was still evident in spite of a 90% reduction in the glycogen peak. The results showed that the glycogen accumulation prior to the enzyme "overshoot" was not obligatory to the subsequent rise in enzyme activity. The sequential accumulation/breakdown of liver glycogen (day 1 refeeding) followed by the accumulation of liver fat (day 2 of refeeding) are probably the result of the changes in enzymatic pathways available to deal with the inflow of excess glucose. Such dissociation of glycogen accumulation and G6PD and ME "overshoot" during starvation-refeeding makes it highly unlikely that either glucose or glucose-6-phosphate derived from glycogen would be the direct, primary inducer of G6PD or ME in rat liver.
对饥饿2天然后喂食高糖、适量蛋白质饮食3天的大鼠，测定其肝脏葡萄糖-6-磷酸脱氢酶（G6PD，EC 1.1.1.49）和苹果酸酶（ME，EC 1.1.1.40）的活性。在再喂食期间，给大鼠注射甲状腺素以在酶“超调”之前阻断糖原积累。尽管糖原峰值降低了90%，但再喂食结束时G6PD和ME的“超调”仍然明显。结果表明，酶“超调”之前的糖原积累对于随后的酶活性升高并非必需。肝脏糖原的顺序积累/分解（再喂食第1天），随后是肝脏脂肪的积累（再喂食第2天），可能是处理过量葡萄糖流入的可用酶促途径变化的结果。在饥饿-再喂食期间糖原积累与G6PD和ME“超调”的这种分离使得糖原衍生的葡萄糖或葡萄糖-6-磷酸极不可能是大鼠肝脏中G6PD或ME的直接、主要诱导剂。
