α, β-Amyrin, a pentacyclic triterpenoid from Protium heptaphyllum suppresses adipocyte differentiation accompanied by down regulation of PPARγ and C/EBPα in 3T3-L1 cells

• Main Authors: Karina Moura de Melo, Francisca Tuelly Bandeira de Oliveira, Rose Anny Costa Silva, Ana Luiza Gomes Quinderé, José Delano Barreto Marinho Filho, Ana Jérsia Araújo, Eanes Delgado Barros Pereira, Adonias Almeida Carvalho, Mariana Helena Chaves, Vietla Satyanarayana Rao, Flávia Almeida Santos
• Format: Article
• Language: English
• Published: Elsevier 2019-01-01
• Series: Biomedicine & Pharmacotherapy
• Subjects: α, β-Amyrin; 3T3-L1 cells; Adipocyte differentiation; PPARγ; C/EBPα; GLUT4
• Online Access: http://www.sciencedirect.com/science/article/pii/S0753332218338654

Previous studies have reported the anti-obesity effects of α, β-Amyrin in high fat-fed mice. This study aimed to evaluate whether α, β-Amyrin has an anti-adipogenic effect in 3T3-L1 murine adipocytes and to explore the possible underlying mechanisms. 3T3-L1 pre-adipocytes were differentiated in a medium containing insulin, dexamethasone, and 1-methyl-3-isobutylxanthine. Cytotoxicity of α, β-Amyrin was assessed by MTT assay. Lipid content in adipocytes was determined by Oil-Red O staining. In addition, the protein expression levels of peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer binding proteins alpha (C/EBPα), beta (C/EBPβ), and delta (C/EBPδ) and glucose transporter 4 (GLUT4) were determined by qRT-PCR and western blot analysis. Oil-Red O staining revealed markedly reduced fat accumulation by α, β-Amyrin (6.25–50 μg/mL) without affecting cell viability. Furthermore, our results indicate that α, β-Amyrin can significantly suppress the adipocyte differentiation by downregulating the expression levels of adipogenesis-related key transcription factors such as PPARγ and C/EBPα, but not C/EBPβ or C/EPBδ. In addition, the protein expression of membrane GLUT4 in 3T3- L1 adipocytes treated with α, β-Amyrin was significantly higher than in control cells, indicating that α, β-Amyrin augments glucose uptake. These findings suggest that α, β-Amyrin exerts an anti-adipogenic effect principally via modulation of lipid and carbohydrate metabolism in 3T3-L1cells. The present in vitro findings, taken together with our earlier observation of the anti-obesity effect in vivo, suggest that α, β-Amyrin can be developed as a new therapeutic agent for treatment and prevention of obesity.