The effect of high-amylose resistant starch on the glycogen structure of diabetic mice.

Glycogen is a complex branched glucose polymer found in many tissues and acts as a blood-glucose buffer. In the liver, smaller β glycogen particles can bind into larger composite α particles. In mouse models of diabetes, these liver glycogen particles are molecularly fragile, breaking up into smaller particles in the presence of solvents such as dimethyl sulfoxide (DMSO). If this occurs in vivo, such a rapid enzymatic degradation of these smaller particles into glucose could exacerbate the poor blood-glucose control that is characteristic of the disease. High-amylose resistant starch (RS) can escape digestion in the small intestine and ferment in the large intestine, which elicits positive effects on glycemic response and type 2 diabetes. Here we postulate that RS would help attenuate diabetes-related liver glycogen fragility. Normal maize starch and two types of high-amylose starch were fed to diabetic and non-diabetic mice. Molecular size distributions and chain-length distributions of liver glycogen from both groups were characterized to test glycogen fragility before and after DMSO treatment. Consistent with the hypothesis that high blood glucose is associated with glycogen fragility, a high-amylose RS diet prevented the fragility of liver-glycogen α particles. The diets had no significant effect on the glycogen chain-length distributions.