Final answer:
Adrenaline activates GPCRs in muscle cells, causing an increase in cAMP, which activates PKA. PKA phosphorylates enzymes that lead to glycogen breakdown for glucose supply during the fight-or-flight response.
Step-by-step explanation:
GPCR-PKA Signaling in Glycogen Breakdown
The short-term stress response initiated by the hormone adrenaline, also known as epinephrine, involves the activation of G-protein-coupled receptors (GPCRs) in muscle cells. When adrenaline binds to these receptors, it triggers a signaling cascade leading to an increase in cyclic AMP (cAMP) levels. Cyclic AMP then activates protein kinase A (PKA), which phosphorylates two key enzymes in the glycogen breakdown pathway.
The first enzyme is glycogen phosphorylase kinase (GPK), which activates glycogen phosphorylase (GP), leading to the breakdown of glycogen into glucose-1-phosphate. The second enzyme is glycogen synthase (GS), whose phosphorylation inhibits its ability to synthesize glycogen from glucose units, thereby preventing a futile cycle of glycogen synthesis and breakdown. This process ensures that muscle cells have a readily available supply of glucose for energy during the fight-or-flight response.
In summary, adrenaline-induced signaling through the activation of a GPCR leads to PKA activation and a cascade of phosphorylation events, culminating in the rapid breakdown of glycogen into glucose, providing energy for immediate physical exertion.