Final answer:
In adrenaline's presence, muscle cells lacking GPCR would have higher glycogen levels compared to those with functional receptors, due to the inability to trigger the signaling pathway that leads to glycogen breakdown.
Step-by-step explanation:
In the presence of adrenaline, muscle cells without the G-protein-coupled receptor (GPCR) would have higher glycogen levels compared to normal muscle cells treated with adrenaline. Normally, when adrenaline (also known as epinephrine) binds to the GPCR in muscle cells, it triggers a cascade of events resulting in the production of cyclic AMP (CAMP). CAMP activates protein kinase A (PKA), which phosphorylates enzymes involved in glycogen breakdown, leading to glycogen degradation and inhibition of glycogen synthesis. Hence, muscle cells that lack GPCR would not be able to respond to adrenaline, and the breakdown of glycogen into glucose would be reduced, resulting in higher glycogen levels within these cells.
The summary of the signaling pathway is as follows: adrenaline binds to GPCR, leading to G-protein activation of adenylyl cyclase; this results in the conversion of ATP to CAMP. Subsequently, CAMP activates PKA, which then promotes glycogen breakdown and inhibits glycogen synthesis.