Diurnal changes of glycogen molecular structure in healthy and diabetic mice

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.