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. Author manuscript; available in PMC: 2017 Nov 28.
Published in final edited form as: J Intern Med. 2014 May 27;276(6):543–559. doi: 10.1111/joim.12268

Figure 4. Acute activation of fatty acid oxidation and inhibition of fatty acid synthesis by AMPK.

Figure 4

AMPK phosphorylates both isoforms ACC1 and ACC2 at equivalent sites (Ser80 and Ser221 in human ACC1 and ACC2 respectively), causing their inactivation. This lowers malonyl-CoA, a key intermediate in fatty acid synthesis that is also an inhibitor of carnitine palmitoyl transferase-1 (CPT1). CPT1 is involved in uptake of fatty acids into mitochondria, where they are oxidized to generate ATP. It was thought that ACC1 produced the pool of malonyl-CoA involved in fatty acid synthesis, and ACC2 a separate pool of malonyl-CoA that regulates CPT1 [117], but recent results suggest that these two pools cannot be completely distinct [77].