Glikogenolisis

Glikogenolisis, also known as glycogenolysis, is a metabolic pathway that breaks down glycogen into glucose, providing a readily available energy source for cells. This process primarily occurs in the liver and skeletal muscles, where glycogen serves as an energy reserve. The breakdown of glycogen is essential for maintaining blood glucose levels, particularly during periods of fasting or intense physical activity.

The pathway begins with the enzyme glycogen phosphorylase, which catalyzes the cleavage of glycogen into glucose-1-phosphate. This reaction occurs at the non-reducing ends of glycogen branches, progressively shortening the glycogen molecule. The glucose-1-phosphate is then converted into glucose-6-phosphate by the enzyme phosphoglucomutase. In the liver, glucose-6-phosphate can be further dephosphorylated by glucose-6-phosphatase to release free glucose into the bloodstream, thereby increasing blood glucose levels. In muscle cells, glucose-6-phosphate remains within the cell to fuel glycolysis or other metabolic processes.

Glikogenolisis is tightly regulated by hormonal and allosteric mechanisms. Glucagon and epinephrine stimulate glycogenolysis by activating glycogen phosphorylase through a cascade of phosphorylation events mediated by protein kinases. Conversely, insulin inhibits glycogenolysis by promoting the dephosphorylation of glycogen phosphorylase, thereby reducing its activity. Allosteric regulation also plays a role, with ATP and glucose acting as inhibitors of glycogen phosphorylase, while AMP and glucose-6-phosphate stimulate the enzyme.

Disruptions in glycogenolysis can lead to metabolic disorders, such as glycogen storage diseases, where defects in enzymes involved in the pathway result in abnormal glycogen accumulation or impaired glucose release. These conditions often require dietary management or enzyme replacement therapies to mitigate symptoms.