Effect of Black Soybean Koji Extract on Glucose Utilization and Adipocyte Differentiation in 3T3-L1 Cells

International Journal of Molecular Sciences

Chi-Chang Huang³  Wen-Ching Huang⁴  Chien-Wen Hou²  Yu-Wei Chi¹ 

[1] Department of Food Science, Nutrition, and Nutraceutical Biotechnology, Shih Chien University, Taipei 10462, Taiwan; E-Mail:;Department of Sports Sciences, University of Taipei, Taipei 11153, Taiwan; E-Mail:;Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 33301, Taiwan; E-Mail:;Graduate Institute of Athletics and Coaching Science, National Taiwan Sport University, Taoyuan 33301, Taiwan; E-Mail:

关键词: black soybean koji;    3T3-L1 preadipocytes;    insulin;    adipokines;   

DOI  :  10.3390/ijms15058280

来源: mdpi

【 摘 要 】

Adipocyte differentiation and the extent of subsequent fat accumulation are closely related to the occurrence and progression of diseases such as insulin resistance and obesity. Black soybean koji (BSK) is produced by the fermentation of black soybean with Aspergilllus awamori. Previous study indicated that BSK extract has antioxidative and multifunctional bioactivities, however, the role of BSK in the regulation of energy metabolism is still unclear. We aimed to investigate the effect of glucose utilization on insulin-resistant 3T3-L1 preadipocytes and adipogenesis-related protein expression in differentiated adipocytes with BSK treatment. Cytoxicity assay revealed that BSK did not adversely affect cell viability at levels up to 200 μg/mL. The potential for glucose utilization was increased by increased glucose transporter 1 (GLUT1), GLUT4 and protein kinase B (AKT) protein expression in insulin-resistant 3T3-L1 cells in response to BSK treatment. Simultaneously, BSK inhibited lipid droplet accumulation in differentiated 3T3-L1 cells. The inhibitory effect of adipogenesis was associated with downregulated peroxisome proliferator-activated receptor γ (PPARγ) level and upregulated Acrp30 protein expression. Our results suggest that BSK extract could improve glucose uptake by modulating GLUT1 and GLUT4 expression in a 3T3-L1 insulin-resistance cell model. In addition, BSK suppressed differentiation and lipid accumulation in mature 3T3-L1 adipocytes, which may suggest its potential for food supplementation to prevent obesity and related metabolic abnormalities.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland