Figure 2.Proposed mechanism for how the PKA Cβ deletion
results in resistance to obesity, fatty liver, and heart disease.
Activation of AMPK is known to affect different aspects of lipid metabolism,
and to play a role in protein synthesis. PKA inhibits activity of AMPK, and
we have shown that loss of Cβ results in decreased levels of ChREBP.
Our model proposes that disruption of Cβ and concomitant increased AMPK
activity leads to a decrease in fatty acid and protein synthesis and an
increase in lipolysis and fatty acid oxidation in select tissues. Leptin
sensitivity caused by disruption of Cβ may also play a role in the
observed increase in AMPK activity in our mutants. A compensatory increase
by Cα in the brain also results in an increase in overall energy
expenditure.
