1998/11/15 by Mathieu Bollen, Mathieu BOLLEN, Stefaan KEPPENS +3 · 1 citation
Biochemistry, Genetics and Molecular Biology · Medicine · #Adenosine and Purinergic Signaling #Glycogen Storage Diseases and Myoclonus #Pancreatic function and diabetes
paper · pdf · doi:10.1042/bj3360019
openalex publication_date 1998/11/15 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
Although the general pathways of glycogen synthesis and glycogenolysis are identical in all tissues, the enzymes involved are uniquely adapted to the specific role of glycogen in different cell types. In liver, where glycogen is stored as a reserve of glucose for extrahepatic tissues, the glycogen-metabolizing enzymes have properties that enable the liver to act as a sensor of blood glucose and to store or mobilize glycogen according to the peripheral needs. The prime effector of hepatic glycogen deposition is glucose, which blocks glycogenolysis and promotes glycogen synthesis in various ways. Other glycogenic stimuli for the liver are insulin, glucocorticoids, parasympathetic (vagus) nerve impulses and gluconeogenic precursors such as fructose and amino acids. The phosphorolysis of glycogen is mainly mediated by glucagon and by the orthosympathetic neurotransmitters noradrenaline and ATP. Many glycogenolytic stimuli, e.g. adenosine, nucleotides and NO, also act indirectly, via secretion of eicosanoids from non-parenchymal cells. Effectors often initiate glycogenolysis cooperatively through different mechanisms.