## 1 Introduction  
Enlarged adipocytes and excess adiposity play a key role in the metabolic and cardiovascular complications associated with obesity [1]. Our current understanding is that hypertrophic obesity is strongly associated with obesity-related insulin resistance and type 2 diabetes (T2D), while hyperplastic obesity is not usually linked to these metabolic consequences, which are seen in 20-30% of obese individuals characterized as \"obese but metabolically normal\" [2; 3; 4; 5]. This clearly suggests that impaired formation of new adipocytes through preadipocyte differentiation (i.e., adipogenesis) is linked to the pathological expansion of adipose tissue (AT), as evidenced by decreases in insulin sensitivity and expression of mRNAs by differentiation markers such as peroxisome proliferator-activated receptor (PPAR\(\gamma\)), glucose transporter 4 (GLUT4), and adiponectin [6; 7]. Moreover, a hypertrophic environment also leads to AT dysfunction by impairing adipocyte insulin signaling pathways, thereby promoting insulin resistance [8; 9]. Consequently, the hyperplastic expansion of adipocytes over hypertrophic enlargement within an individual can counteract the negative metabolic effects of obesity, and has an enormous impact on metabolic health outcomes. Accordingly, adipocytes have recently been emerging as a therapeutic target for obesity-associated metabolic disorders and thus introducing agents that promote preadipocyte differentiation and/or lipid oxidation would be a promising strategy for obesity-induced metabolic disorders. _Panax ginseng_ Meyer is believed to be a panacea, used in traditional oriental medicine for over 2000 years primarily to enhance physical and mental performance [10; 11]. The pharmacological properties of ginseng and its constituents depend on the type and site of the attached sugar moieties, and have been largely attributed to ginseng [12; 13; 14]. Historically, raw ginseng is processed into either white ginseng by a simple drying method or red ginseng by a steaming process to enhance its shelf-life and efficacy [15; 16; 17]. Red ginseng is known to have a distinct ginseng profile compared to white and raw ginseng in the content and composition of ginsenosides [18; 19; 20]. In particular, red ginseng is shown to be rich in ginsenoside Rg3, which is significantly increased during the steaming process, whereas ginsenoside Rb1, the most abundant ginsenoside in ginseng root, is relatively reduced in steamed red ginseng [15; 20; 21; 22; 23]. Recent studies have shown that ginsenoside Rb1 is deglycosylated by human intestinal bacteria or digestive enzymes and is converted to a minor metabolite form, Rg3 [24; 25]. It is also reported that deglycosylated ginseng metabolites are more readily absorbed into the blood stream and thus act as biologically active compounds [26]. Clinical and pre-clinical studies have also shown that ginseng extract and ginsenosides exert anti-diabetic effects by lowering blood glucose levels and enhancing insulin sensitivity [27; 28]. Similarly, ginsenosides Rb1 and Rg3 have been reported to possess anti-diabetic effects, mainly through blood glucose control in animals and the stimulation of glucose uptake in 3T3-L1 mature adipocytes and L6 myotubes [29; 30; 31; 32; 33; 34]. However, there have been contradictory results that Rb1 induces adipocyte differentiation, whereas Rg3 inhibits it, which may be due to the differences in the concentrations of ginsenosides and different cell culture models used in various studies [30; 34; 35; 36; 37; 38]. In addition, no comparative studies have been reported for the potential bioactivity of Rb1 in combination with its metabolite, Rg3. The aim of this study was to investigate the effect of the individual, as well as the combination of, ginsenosides Rb1 and Rg3 on adipocyte differentiation, glucose transport systems, adiponectin, and the insulin signaling pathway using a well-established model of adipocyte differentiation, 3T3-L1 preadipocytes.