Abstract
Liver fibrosis (LF) leads to liver failure and short survival. Liver glycogen is a hyperbranched glucose polymer, comprising individual β particles, which can bind together to form aggregated α particles. Glycogen functionality depends on its molecular structure. This study compared the molecular structure of liver glycogen from both LF and healthy rats, and explored underlying mechanisms for observed differences. Glycogen from both groups contained α and β particles; the LF group contained a higher proportion of β particles, with the glycogen containing fewer long chains than seen in the control group. Both glycogen branching enzyme and glycogen phosphorylase showed a significant decrease of activity in the LF group. Transcriptomics and proteomics revealed a functional deficiency of mitochondria in the LF group, which may lead to changes in glycogen structure. These results provide for the first time an understanding of how liver fibrosis affects liver glycogen metabolism and glycogen structure. HYPOTHESIS: We hypothesized that the molecular structure of liver glycogen from a rat model of liver fibrosis would be altered compared to the control group.