Dietary acetic acid is metabolized to acetyl-CoA with the production of AMP [4], which, in vitro, results in the elevation of the AMP/ATP ratio and subsequent phosphorylation of AMPK [5]. Based on these findings, previous studies found that dietary acetic acid suppressed body fat accumulation in animals by regulating genes for energy consumption and fatty acid oxidation enzymes in liver [6]. However, the effects of dietary acetic acid on AMPK activation in adipose tissue remains relatively unexplored, although AMPK is ubiquitously expressed and plays an important role in various physiological and pathological processes in the liver and adipose tissue [7]. Furthermore, little information is available on the coordinated control of lipid metabolism through the phosphorylation of each AMPK protein and its downstream effectors in the liver and adipose tissue