Glycogen is a complex branched glucose polymer functioning as a blood-sugar reservoir in animals. Liver glycogen β particles can bind together to form α particles, which have a slower enzymatic degradation to glucose. The linkage between β particles in α particles in diabetic liver breaks (is fragile) in dimethyl sulfoxide (DMSO), a H-bond disruptor, consistent with blood-sugar homeostasis loss in diabetes. We examined diurnal changes in the molecular structure of healthy and diabetic mouse-liver glycogen. Healthy mouse glycogen was fragile to DMSO during glycogen synthesis but not degradation; diabetic glycogen was always fragile. Two alternative mechanisms for this are suggested: healthy glycogen is fragile when formed and becomes stable during subsequent degradation, a process damaged in diabetes; alternatively, there are two types of glycogen: one compact but fragile and the other loose but non-fragile. This suggests potential types of diabetes drug targets through modifying the activities of glycogen synthesis enzymes.

糖原是一种复杂的支链葡萄糖聚合物，在动物中起着血糖储存的作用。肝糖原β颗粒可以结合在一起形成α颗粒，其对葡萄糖的酶促降解速度较慢。糖尿病肝脏中α颗粒中的β颗粒之间的联系在二甲基亚砜（DMSO）（一种氢键破坏剂）中断裂（易碎），与糖尿病患者血糖稳态的损失一致。我们检查了健康和糖尿病小鼠肝脏糖原分子结构的日变化。健康的小鼠糖原在糖原合成过程中对DMSO脆弱，但不降解。糖尿病糖原总是脆弱的。提出了两种替代的机制：健康的糖原形成时很脆弱，在随后的降解过程中变得稳定，这在糖尿病中是受损的。或者，糖原有两种类型：一种紧凑但易碎，而另一种宽松但不易碎。这表明，通过修饰糖原合成酶的活性，可能成为糖尿病药物靶标的潜在类型。