Figure 1.

Schematic overview of mitochondrial energy transduction within a brown adipocyte mitochondrion. Norepinephrine (NE) activation of adrenergic receptors (AR) causes an increase in cytosolic cyclic adenosine monophosphate (cAMP) levels. The subsequent activation of lipases results in the lipolysis of triacylglycerol (TAG), which increases intracellular free fatty acid (FFA) concentrations. FFAs fulfill two principal metabolic fates: (i) FFAs bind to and activate uncoupling protein 1 (UCP1), thus switching on UCP1-mediated proton (H⁺) conductance. (ii) Activated FFAs (acyl-CoA) can be transported into the mitochondrion via the carnitine palmitoyl transferase (CPT) system and be oxidized to acetyl-CoA, thereby potentiating anaplerosis and providing reducing equivalents for the electron transport chain (ETC). Pyruvate also participates in mitochondrial anaplerosis and the production of reducing equivalent by being decarboxylated to acetyl-CoA by pyruvate dehydrogenase (PDH) or being carboxylated by pyruvate carboxylase (PC), forming oxaloacetate (OAA).