Suppression of Adipogenesis and Fat Accumulation by Vitexin Through Activation of Hedgehog Signaling in 3T3-L1 Adipocytes

Many studies have demonstrated that adipogenesis is associated with obesity, and the Hedgehog (Hh) signaling pathway regulates adipogenesis and obesity. Following the screening study of the chemical library evaluating the effect of vitexin on Gli1 transcriptional activity, vitexin was chosen as a candidate for antiadipogenic efficacy. Vitexin significantly reduced lipid accumulation and suppressed C/EBP alpha (CCAAT/enhancer-binding protein alpha) and PPAR gamma (peroxisome proliferator-activated receptor gamma) expression, which are known as key adipogenic factors in the early stages of adipogenesis by activating Hh signaling. Furthermore, Hh inhibitor GANT61 reversed the effect of AMP-activated protein kinase (AMPK) activator AICAR (5-aminoimidazole-4-carboxamide ribonucleotide), indicating that Hh signaling is an upstream regulator of AMPK in 3T3-L1 cells. Vitexin suppressed adipogenesis by regulating Hh signaling and phosphorylation of AMPK, leading to the inhibition of fat formation. These results suggest that vitexin can be considered a potent dietary agent in alleviating lipid accumulation and obesity.

Automated summary

Studies have shown that vitexin can suppress adipogenesis by regulating the Hh signaling pathway and phosphorylation of AMPK, which leads to reduced lipid accumulation and obesity.