Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cells.
Choi SS., Cha BY., Lee YS., Yonezawa T., Teruya T., Nagai K.
Animal Study on Type 2 Diabetes, published in Life Sci (2009) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Life Sci (2009)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 19376135
- DOI
- 10.1016/j.lfs.2009.04.001
Abstract (original English)
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. 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. 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
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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