Acetate stimulates lipogenesis via AMPKα signaling in rabbit adipose-derived stem cells

Acetate plays an important role in host lipid metabolism. However, the regulatory network underlying acetate-regulated lipometabolism remains unclear. The aim of this study was to determine whether any cross talk occurs among adenosine 5'-monophosphate-activated protein kinase (AMPK), mitogen-activated protein kinases (MAPKs) and acetate in regulating lipid metabolism. The compound C (an AMPK inhibitor), and SB203580 (a p38 MAPK inhibitor) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively. It indicated that acetate (6 mM) for 6 h increased the lipid deposition in rabbit ADSCs. Besides, acetate treatment (6 mM) increased significantly phosphorylated protein level of AMPKα and p38 MAPK, but not altered significantly the phosphorylated protein level of extracellular signaling-regulated kinase (ERK) and c-Jun aminoterminal kinase (JNK). The blocking of AMPKα signaling attenuated acetate-induced lipid accumulation, but not that of p38 MAPK signaling. In conclusion, our findings suggest that AMPKα signaling pathway is associated with acetate-induced lipogenesis.