Gilbert M, Bourbon J
Diabetes. 1980 Apr;29(4):266-71. doi: 10.2337/diab.29.4.266.
The effects of variations of glycemia from 1.7 to 35 mM on the activity of glycogen synthase and phosphorylase, on glycogen content, and on U-14C-glucose incorporation into glycogen in the liver of the near-term rat fetus were investigated. Hypoglycemia did not affect the activities of phosphorylase and synthase; total glycogen content was not modified, but incorporation of labeled glucose was markedly decreased. This is consistent with a decreased glycogen synthesis. A slight hyperglycemia (about 5.5 mM) sharply decreased phosphorylase a (active) activity but increased slightly glycogen synthase a activity; liver glycogen content and labeled glucose incorporation were both enhanced. Higher levels of glycemia induced a decrease of phosphorylase a activity of the same order, but by contrast, glycogen synthase a activity increased progressively with increasing glycemia. Sequential study showed that hyperglycemia first induced the decrease of phosphorylase activity, then increased synthase activity. Marked hyperglycemia strongly enhanced liver glycogen content and labeled glucose incorporation. The fetal liver appears very responsive to acute variations of glycemia. The mechanisms seem to be oriented toward maximal glycogen accumulation.
研究了血糖水平在1.7至35 mM之间变化对近足月大鼠胎儿肝脏中糖原合酶和磷酸化酶活性、糖原含量以及U-14C-葡萄糖掺入糖原的影响。低血糖不影响磷酸化酶和合成酶的活性；总糖原含量未改变，但标记葡萄糖的掺入明显减少。这与糖原合成减少一致。轻度高血糖（约5.5 mM）可使磷酸化酶a（活性形式）活性急剧下降，但糖原合酶a活性略有增加；肝糖原含量和标记葡萄糖掺入均增加。更高水平的血糖导致磷酸化酶a活性出现相同程度的下降，但相反，糖原合酶a活性随血糖升高而逐渐增加。连续研究表明，高血糖首先导致磷酸化酶活性下降，然后合成酶活性增加。显著高血糖强烈增强肝糖原含量和标记葡萄糖掺入。胎儿肝脏似乎对血糖的急性变化非常敏感。其机制似乎倾向于最大程度的糖原积累。
