Department of Anatomy, Histology and Embryology, Medical School, University of Ioannina, Ioannina 45110, Greece.
Microsc Res Tech. 2010 Oct;73(11):1009-14. doi: 10.1002/jemt.20825.
The effects of parenteral administration of glucose, 3-methylglucose (3MG), or 2-deoxyglucose (2DG) on the glycogen autophagy were studied in the newborn rat liver using electron microscopy and biochemical methods. The administration of glucose resulted in hyperglycemia and prevented the mobilization of hepatocytic glycogen. It also prevented the development of autophagic vacuoles in general and inhibited the glycogen-degrading activity of acid α-1,4-glucosidase. The nonphosphorylated and not further metabolized glucose analog 3MG also produced hyperglycemia, but increased acid glucosidase. Pretreating the newborns with the β-adrenergic blocker propranolol inhibited the effects of 3MG. The phosphorylated but not fully metabolized glucose analog 2DG produced similar effects. The administration of xylitol to the newborns already treated with 2DG, suppressed acid glucosidase. The results of this and our previous studies suggest that glucose must be metabolized beyond its phosphorylation step to inhibit acid glucosidase activity.
本研究采用电子显微镜和生化方法，观察了新生大鼠肝脏经静脉给予葡萄糖、3-甲基葡萄糖（3MG）或 2-脱氧葡萄糖（2DG）后，对其肝糖原自噬的影响。葡萄糖的给予导致高血糖，并阻止了肝细胞糖原的动员。它还阻止了自噬小泡的一般发展，并抑制了酸性α-1,4-葡萄糖苷酶的糖原降解活性。非磷酸化且未进一步代谢的葡萄糖类似物 3MG 也会导致高血糖，但会增加酸性葡萄糖酶。用β-肾上腺素能阻滞剂普萘洛尔预处理新生大鼠，可抑制 3MG 的作用。已磷酸化但未完全代谢的葡萄糖类似物 2DG 也产生了类似的效果。给予新生大鼠 2DG 已处理的木糖醇可抑制酸性葡萄糖酶。本研究及以往研究结果表明，葡萄糖必须在其磷酸化步骤之后进一步代谢，才能抑制酸性葡萄糖酶的活性。
