Diurnal changes of glycogen molecular structure in healthy and diabetic mice. (1st April 2018)

• Record Type: Journal Article
• Authors: Hu, Zhenxia; Deng, Bin; Tan, Xinle; Gan, Hua; Li, Cheng; Nada, Sharif S.; Sullivan, Mitchell A.; Li, Jialun; Jiang, Xiaoyin; Li, Enpeng; Gilbert, Robert G.
• Is Part Of: Carbohydrate polymers. Volume 185(2018)
• Page Start: 145
• Page End: 152
• Publication Date: 2018-04-01
• Subjects: Glycogen -- Molecular structure -- Characterization -- Diabetes -- GPC; Polysaccharides -- Periodicals; Polysaccharides -- Periodicals; Polysaccharides -- Périodiques; Electronic journals; 547.78
• DOI: 10.1016/j.carbpol.2018.01.003
• Languages: English
• ISSNs: 0144-8617

Abstract

Highlights: Glycogen is complex branched glucose polymer, reservoir for blood sugar in animals. Has multi-level structure, including bound aggregates of smaller glycogen molecules. This binding is fragile in diabetic liver glycogen. Data on fragility as a function of time after feeding suggests biosynthesis mechanism. Molecular origin of fragility suggests it arises from glycogen biosynthesis enzymes. Abstract: 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.