Butein inhibits adipocyte differentiation by modulating the AMPK pathway in 3T3‐L1 cells
Publisher：
John Wiley & Sons Inc
E-ISSN：
1745-4514|42|1|jfbc.12441-jfbc.12441
ISSN：
0145-8884
Source：
JOURNAL OF FOOD BIOCHEMISTRY (ELECTRONIC),
Vol.42,
Iss.1, 2018-02,
pp. : n/a-n/a
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Abstract
AbstractButein (3,4,2ʹ,4ʹ‐tetrahydroxychalcone), a chalcone derivative, has been reported to exhibit various biological effects. However, the inhibitory effects of butein on adipocyte differentiation mediated via the adenosine 5ʹ‐monophosphate‐activated protein kinase (AMPK) signaling pathway have not been investigated. This study elucidated the effects of butein treatment on adipogenesis regulated by the AMPK pathway using the 3T3‐L1 cells. Butein inhibited lipid accumulation by regulating the early phase events of adipogenesis, and suppressed the expression of adipogenic transcription factors and their downstream target genes. Furthermore, AMPK and acetyl‐CoA carboxylase (ACC) were significantly phosphorylated upon butein treatment in 3T3‐L1 cells. The anti‐adipogenic effects of butein were mediated by the activation of AMPK which was confirmed by using compound C, a highly specific inhibitor of AMPK. Butein also modulated enzymes involved in fatty acid metabolism such as ACC, carnitine palmitoyl transferase‐1 (CPT‐1), and glycerol‐3‐phosphate acyl transferase (GPAT)‐1.Practical applicationsButein decreased lipid accumulation and adipocyte differentiation mediated via the AMPK signaling pathway in 3T3‐L1 adipocytes. Based on these findings, it is suggested that butein may possess therapeutic potential for prevention and treatment of obesity and obesity‐related diseases.
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