Compound K, a Panax ginseng saponin, inhibits lipid accumulation during adipocyte differentiation by regulating early adipogenic genes

Abstract

Compound K (20‐O‐β‐(D‐glucopyranosyl)‐20 (S)‐protopanaxadiol, CK) is one of the major panaxadiol ginsenosides in Panax ginseng. CK has been known to have various biological properties such as anti‐inflammation, anti‐diabetes and anti‐tumor. In this study, we investigated anti‐adipogenic effect of CK during adipogenesis in 3T3‐L1 cell. CK suppressed lipid accumulation during adipogenesis in a dose‐dependent manner (10, 25, 50 μM) in Oil red O staining assay. This inhibition was evidenced by the downregulation of triacylglycerol synthetic proteins such as Glycerol‐3‐ phosphate acyltransferase3 (GPAT3), 1‐acylglycerol‐3‐phosphate acyltransferase2 (AGPAT2), Lipin1 and Diacylglycerol acyltransferase1 (DGAT1). Our data also showed that the inhibitory action of CK was usually limited to early stage of adipogenesis. This result was correlated to the reduction in mRNA levels of the early adipogenic factors, Krueppel‐like factor4 (KLF4), Early growth response2 (EGR2), CCAAT/enhancer‐binding protein beta (C/EBPβ), and C/EBPδ. In contrast, mRNA expression of a negative regulator of early adipogenesis, KLF2, was increased with a CK treatment. CK‐induced regulation of early adipogenic genes led to the reduction in the expression of the late adipogenic transcription factors such as peroxisome proliferator activated receptor gamma (PPARγ) and C/EBPα, and their target gene, Fatty acid binding protein4 (FABP4). Collectively, our study suggests that CK is an inhibitory edible compound on adipogenesis and TG synthesis.Grant Funding Source: Korea and National Research Foundation of Korea