Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cells

Abstract

Aims The nuclear receptor peroxisome proliferator-activated receptor (PPAR) γ plays an important role in adipocyte differentiation. Its ligands, including thiazolidinediones, improve insulin sensitivity in type 2 diabetes. We investigate the effect of magnolol, an ingredient of Magnolia officinalis on adipogenesis and glucose uptake using 3T3-L1 cells. Main methods The effect of magnolol on adipocyte differentiation was quantified by measuring Oil Rd O staining using 3T3-L1 cells and C3H10T1/2 cells. And real-time PCR and western blot were used to determine the expression of PPARγ or PPARγ target genes, respectively. The effect of magnolol on glucose uptake was performed using 3T3-L1 adipocytes. Key findings Magnolol dose-dependently enhanced adipocyte differentiation in 3T3-L1 cells and C3H10T1/2 cells. In the early stage of adipogenesis, magnolol induced gene expression of C/EBPδ, C/EBPα and PPARγ2 and during adipocyte differentiation, it also induced the expression of PPARγ target genes such as aP2, LPL and adiponectin. In addition, magnolol it also increase expression of PAPRγ target gene such as C/EBPα and aP2 at mRNA and aP2 protein level in mature adipocytes. In PPARγ ligand binding assays, magnolol exhibited binding affinity to PPARγ but its activity was weaker than rosiglitazone. At the same time, magnolol-induced adipogenesis was inhibited by co-treatment of GW9662 both 3T3-L1 cells and C3H10T1/2 cells. In mature 3T3-L1 adipocytes, magnolol increased basal and insulin-stimulated glucose uptake accompanied by the up-regulation of mRNA and protein level of Glut4. Significance Our results suggest that magnolol could improve insulin sensitivity through the activation of PPARγ as a ligand.