Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cells.
OBJECTIVE
The nuclear receptor peroxisome proliferator-activated receptor (PPAR) gamma 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.


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 PPARgamma or PPARgamma target genes, respectively. The effect of magnolol on glucose uptake was performed using 3T3-L1 adipocytes.


RESULTS
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/EBPdelta, C/EBPalpha and PPARgamma2 and during adipocyte differentiation, it also induced the expression of PPARgamma target genes such as aP2, LPL and adiponectin. In addition, magnolol it also increase expression of PAPRgamma target gene such as C/EBPalpha and aP2 at mRNA and aP2 protein level in mature adipocytes. In PPARgamma ligand binding assays, magnolol exhibited binding affinity to PPARgamma 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.


CONCLUSIONS
Our results suggest that magnolol could improve insulin sensitivity through the activation of PPARgamma as a ligand.
Choi
Sun-Sil
SS
Research Institute for Biological Functions, Chubu University, 1200 Matsumoto, Kasugai, Aichi, Japan.
Cha
Byung-Yoon
BY
Lee
Young-Sil
YS
Yonezawa
Takayuki
T
Teruya
Toshiaki
T
Nagai
Kazuo
K
Woo
Je-Tae
JT
D041721:3T3-L1 Cells / Q000166:cytology / Q000378:metabolism; D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism; D000818:Animals; D001713:Biphenyl Compounds / Q000378:metabolism / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D005786:Gene Expression Regulation; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D008024:Ligands; D017705:Lignans / Q000378:metabolism / Q000494:pharmacology*; D031566:Magnolia / Q000737:chemistry; D051379:Mice; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics / Q000378:metabolism*; D039904:Pluripotent Stem Cells / Q000166:cytology / Q000378:metabolism; D011485:Protein Binding; D012333:RNA, Messenger / Q000235:genetics
D001713:Biphenyl Compounds; D007328:Insulin; D008024:Ligands; D017705:Lignans; D047492:Peroxisome Proliferator-Activated Receptors; D012333:RNA, Messenger; C005498:magnolol; D005947:Glucose