When the steady state level of cAMP rises, the AMP:ATP ratio in a cell also increases.
“In cardiomyocytes, β2-AR stimulation resulted in a reduction in ATP production but was accompanied by a rise in its precursor, AMP … The AMP/ATP ratio was enhanced …, which subsequently led to the activation of AMP-activated kinase (AMPK)….Lietal2010(JPhysiol).
This activates AMP kinase, which phosphorylates TSC2 and RAPTOR, a subcomplex of mTORC1, and de-activates mTORC1. mTORC1 is a protein complex that is activated by nutrients and growth factors, and it is of importance in neurodegeneration. Together with PDK1, it activates S6K1, which stimulates protein synthesis by the ribosomal protein S6. S6K1 and mTORC1 are caught in a positive feedback loop.
In other words we have a complex integration of signals that converge on the ribosome in order to influence protein synthesis by sensing energy levels in the cell. Basically, AMPK decreases protein synthesis (mTORc1).
Under optimal physiological conditions, the AMP-to-ATP ratio is maintained at a level of
(*) Hardie DG and Hawley SA. AMP-activated protein kinase: the energy
charge hypothesis revisited. Bioessays 23: 1112–1119, 2001..
And here is something entirely different: sensing ph-levels.
“Intracellular acidification, another stimulator of in vivo
cAMP synthesis, but not glucose, caused an increase in
the GTP/GDP ratio on the Ras proteins.” (RollandFetal2002)
So there is a lot that is very interesting about cAMPs connection to cellular state sensing, and mediating between cellular state and protein synthesis.