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Daidzein stimulates glucose uptake through activation of PPARγ in 3T3‐L1 adipocytes

Recent studies have shown that soy isoflavones favorably alter metabolic phenotypes associated with type 2 diabetes. However, the insulin‐sensitizing effects of soy isoflavones are unclear. We have previously reported that daidzein, one of major isoflavones, enhanced differentiation, glucose uptake and translocation of GLUT4 protein in 3T3‐L1 adipocytes. Given the role of PPARγ in adipocyte differentiation and insulin sensitivity, we investigated the effects of daidzein on the differentiation, PPARγ activity, and PPARγ‐dependent downstream responses. A PPAR‐responsive reporter gene was transiently cotransfected with PPARγ expression plasmids in 3T3‐L1 cells. Compared to control, daidzein significantly increased transcriptional activity of PPARγ in a dose‐dependent manner (3 and 4.2‐fold at 10 and 20 μM, respectively). Furthermore, the daidzein‐enhanced adipocyte differentiation was markedly inhibited by a PPARγ antagonist (BADGE). We also examined whether the potentiating effects of daidzein on glucose uptake in adipocytes were mediated via PPARγ. The daidzein‐enhanced glucose uptake correlated with an increase in total cellular and plasma membrane expression of GLUT4 protein as well as GLUT4 mRNA. Combination of daidzein and BADGE (100 μM) completely abrogated daidzein‐induced glucose uptake as well as GLUT4 protein abundance. These results indicate that the mechanism by which daidzein increases glucose uptake may be accounted for upregulation of GLUT4 expression through PPARγ activation.