Abstract:

Objective: To investigate the anti-adipogenic effect and underlying mechanism of genistein in 3T3-L1 cells
and its estrogen receptor (ER) mediated pathway. Methods: After treated with various concentrations of genistein, the
survival rate of 3T3-L1 cells was assessed by MTT assay. In addition, after treated with genistein, genistein-ICI182780,
or estrogen, differentiation degree and lipid accumulation of the cells were assessed by oil red staining and a TG assay kit,
and adipocyte lipolysis was assessed by a glycerin assay kit. After intervention by genistein or genistein-ICI182780, the
expression of extracellular signal-regulated kinase (ERK), phospho-extracellular signal-regulated kinase (p-ERK), adenosine
monophosphate activated protein kinase (AMPK), phospho-adenosine monophosphate activated protein kinase (p-AMPK),
hormone sensitive lipase (HSL), and fatty acid synthetase (FAS) were analyzed by Western blotting. Results: Genistein and
high-dose estrogen inhibited lipid accumulation of 3T3-L1 and increased lipolysis in adipocytes. The presence of ICI182780
partly decreased both functions of genistein. Furthermore, genistein increased the expression of p-AMPK and HSL, and
decreased the expression of FAS. The presence of ICI182780 could slightly suppress the increase of p-AMPK caused by
genistein intervention. Conclusion: Genistein can inhibit the adipogenesis and differentiation of 3T3-L1 cells via a non-ER
pathway through a mechanism which may be relate to p-AMPK, HSL and FAS.

Key words: genistein, 3T3-L1 cell, phospho-adenosine monophosphate activated protein kinase (p-AMPK), hormone sensitive lipase (HSL), fatty acid synthetase (FAS)