Final answer:
Because of the cumulative effect of all the amplifications that occur in the cell signal transduction pathway, a minimal quantity of epinephrine can cause a large increase in blood glucose levels.
Step-by-step explanation:
A small quantity of epinephrine can trigger a large increase in blood glucose levels due to the amplification of signaling pathways in liver and muscle cells. In the liver cells, epinephrine binds to a G-protein-linked receptor, which activates adenylyl cyclase, leading to an increase in cyclic AMP (cAMP). The cAMP then activates protein kinase A (PKA), which subsequently phosphorylates enzymes that regulate glycogen metabolism.
Specifically, PKA activates glycogen phosphorylase which promotes the conversion of glycogen back into glucose, providing a quick source of energy for the body's 'fight or flight' response. Additionally, PKA phosphorylates glycogen synthase, inhibiting its activity and preventing the formation of glycogen from glucose, ensuring glucose remains available for energy production.
In muscle cells, a similar pathway is initiated by the binding of epinephrine, but the focus is on readily making glucose available for muscle function. The activation of ß-adrenergic receptors by adrenaline leads to an increase in cAMP inside the cell, which activates PKA. This activation results in the phosphorylation of enzymes that accelerate glycogen breakdown and inhibit glycogen synthesis, providing a spike in glucose levels for the muscle cells.
The effect of a hormone-like epinephrine is greatly amplified as the signaling pathway progresses. This ensures that the initial binding of a relatively small number of hormone molecules to receptors leads to the activation of many downstream molecules and reaction processes, resulting in a significant physiological response, such as the increase in blood glucose levels. To regulate this response and prevent overactivation, cAMP is inactive by the action of phosphodiesterase (PDE), which degrades cAMP into inactive molecules.