Phloretin Promotes Adipogenesis via Mitogen-Activated Protein Kinase Pathways in Mouse Marrow Stromal ST2 Cells.

摘要: Phloretin, a glucose transporter (GLUT) inhibitor, has pleiotropic effects. The present study examined the effects of phloretin on commitment marrow stromal cells to adipocytes, using mouse cell line ST2. Oil red O staining showed that treatment with 10⁻100 µM promoted lipid accumulation. Real-time PCR significantly increased expression adipogenic markers, including PPARγ, C/EBPα, fatty acid synthase, acid-binding protein 4, and adiponectin. Western blotting inhibited ERK1/2 JNK but activated p38 MAPK. Treatment MAPK/ERK kinase inhibitor enhanced adipogenesis, similar phloretin. In contrast, MAPK suppressed phloretin-induced adipogenesis. Although phosphorylated AMP-activated (AMPK), co-incubation an AMPK did not block 2-deoxyglucose colorimetric assay siRNA silencing GLUT1 decreased uptake. However, unlike treatment, addition, adipogenesis in knocked-down cells. Taken together, induced by inhibiting activating were independent uptake inhibition. Phloretin may affect energy metabolism influencing adiponectin expression.