Krill oil inhibited adipogenic differentiation by inducing the nuclear Nrf2 expression and the AMPK activity

Abstract

Abstract The current study investigated the antiadipogenic mechanism of krill oil from the 3T3‐L1 adipocytes. The krill oil adhered to the criteria as a food standard by showing 50.8% of the total phospholipid, 5.27% myristic acid, and 1.63% linoleic acid. The lipid accumulation that was measured in the 3T3‐L1 cells using oil red O staining was reduced up to 54% by the krill oil. The krill oil treatment reduced the adipogenic transcription factors by downregulating the sterol regulatory element binding protein 1 (SREBP1) and acetyl‐CoA carboxylase (ACC), phospho‐ACC, and AMP‐activated protein kinase (AMPK) phosphorylation. The current study confirmed that the krill oil inhibited adipogenesis by downregulating SREBP1 and ACC via the upregulation of the AMPK and nuclear factors E2‐related factor 2 (Nrf2) signaling pathway in the 3T3‐L1 adipocytes. These findings suggest that krill oil is a good source of phospholipid and phosphatidylcholine, which could be a potential natural antiobesity ingredient by inhibiting adipogenesis.

Keywords

• adipogenesis
• adipogenic gene
• krill oil
• phosphatidylcholine