Aster yomena (Kitam.) Honda Inhibits Adipocyte Differentiation in 3T3-L1 Cells

Abstract

Background: Obesity has become a global health problem and causes serious complications. In this study, we investigated the effect of ethyl acetate fraction from Aster yomena (Kitam.) Honda (EFAY) on obesity in 3T3-L1 cells. Methods: To examine the effect of EFAY on adipocyte differentiation, we conducted oil red O staining assay in mature adipocytes. 3T3-L1 preadipocytes were differentiated with EFAY (25, 50, and 100 mu g/mL) for 4 days. On day 9 of differentiation, the number of lipid droplets was measured by oil red 0. The underlying mechanisms of the action of EFAY against differentiation in 3T3-L1 cells were investigated using Western blot analysis. Results: In oil red O staining assay, differentiated adipocytes generated massive lipid droplets compared with preadipocytes. However, treatment with EFAY significantly reduced the generation of lipid droplets compared to EFAY non-treated adipocytes. Western blot analysis revealed that EFAY down-regulated adipogenesis-related protein expressions, such as peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding protein (C/EBP) alpha, and c/EBP beta. Furthermore, EFAY down-regulated levels of lipogenesis-related protein expressions such as fatty acid synthase and acetyl-CoA carboxylase. On the contrary, EFAY promoted lipolysis by activating phospho-hormone-sensitive lipase and adipose triglyceride lipase. Phospho-AMP-activated protein kinase (p-AMPK) and phospho-acetyl-CoA carboxylase were up-regulated by treatment of 3T3-L1 cells with EFAY, subsequently up-regulating GLUT4 levels, indicating that EFAY could regulate glucose uptake as well as lipid metabolism. Conclusions: EFAY reduced adipocyte differentiation by suppressing adipogenesis and lipogenesis, and provoking lipolysis and AMPK pathway. These results imply that EFAY could be employed as a natural agent to ameliorate obesity. Copyright (C) 2019, Taiwan Society of Geriatric Emergency & Critical Care Medicine.