Final answer:
Hepatocytes inactivate PK when glucagon levels rise to prevent glycolysis and conserve glucose for release into the bloodstream. This action, along with the breakdown of glycogen and gluconeogenesis, elevates blood glucose levels and is part of a negative feedback system involving glucagon and insulin.
Step-by-step explanation:
When glucagon levels rise in the bloodstream, indicating a need for increased blood glucose levels, it is necessary for hepatocytes to inactivate protein kinase (PK) that is involved in glycolysis, the process of breaking down glucose for energy. Glucagon is released from alpha cells in the pancreas, usually due to low blood glucose levels, such as between meals or during exercise. Its primary function is to raise blood glucose levels through processes like glycogenolysis and gluconeogenesis. Glycogenolysis is the breakdown of glycogen to glucose in the liver, and gluconeogenesis is the generation of glucose from non-carbohydrate precursors.
Inhibiting PK prevents glycolysis, ensuring that glucose is not consumed within the liver cells and is instead available in the bloodstream for peripheral tissues and the brain. Simultaneously, glucagon activates the enzyme glycogen phosphorylase via a phosphorylation cascade involving cAMP and PKA, which promotes the conversion of stored glycogen to glucose in the liver. These actions collectively function within a negative feedback system that works to stabilize blood glucose levels, balancing the effects of insulin.