RESUMO
Glycogen, a complex branched glucose polymer, is responsible for sugar storage in blood glucose homeostasis. It comprises small ß particles bound together into composite α particles. In diabetic livers, α particles are fragile, breaking apart into smaller particles in dimethyl sulfoxide, DMSO; they are however stable in glycogen from healthy animals. We postulate that the bond between ß particles in α particles involves hydrogen bonding. Liver-glycogen fragility in normal and db/db mice (an animal model for diabetes) is compared using various hydrogen-bond breakers (DMSO, guanidine and urea) at different temperatures. The results showed different degrees of α-particle disruption. Disrupted glycogen showed changes in the mid-infra-red spectrum that are related to hydrogen bonds. While glycogen α-particles are only fragile under harsh, non-physiological conditions, these results nevertheless imply that the bonding between ß particles in α particles is different in diabetic livers compared to healthy, and is probably associated with hydrogen bonding.
Assuntos
Ligação de Hidrogênio , Animais , Camundongos , Dimetil Sulfóxido/química , Glicogênio Hepático/metabolismo , Ureia/química , Guanidina/química , Guanidina/farmacologia , Fígado/metabolismo , MasculinoRESUMO
Liver glycogen, a highly branched glucose polymer, is important for blood sugar homeostasis. It comprises α particles which are made of linked ß particles; the molecular structure changes diurnally. In diabetic liver, the α particles are fragile, easily breaking apart into ß particles in chaotropic agents such as dimethyl sulfoxide. We here use size-exclusion chromatography to study how fasting changes liver-glycogen structure in vivo for mice in which type-2 diabetes had previously been induced. Diabetic glycogen degraded enzymatically more quickly in the fasted animals than did glycogen without fasting, with fewer α particles, which however were still fragile. The glycogen had fewer long chains and more shorter chains after fasting. This study gives an overview of the in vivo dynamic changes in α-particles under starvation conditions in both normal and diabetic livers.