## 4 Discussion
In the case of MAPK expression, further research will be required in vivo, but it can be inferred that the effect of IGBP will reduce the conversion of MAPK to the phosphorylated form. In addition, we confirmed that the expression levels of FABP4, adiponectin, leptin, and G6 Pase genes related to adipogenesis were regulated. Among the various lipogenesis mechanisms, the GLUT4 signaling pathway also plays an important role. GLUT4, a glucose transporter, regulates glucose homeostasis and lipogenesis by regulating insulin signaling [34]. The phosphorylation of IRS-1 and PI3K activates AKT and Tre-2/USP6, BUB2, cdc16 domain family member 1 (TBC1D1) phosphorylation to induce glucose uptake [35; 36]. In the present study, the IGBP 2:1 mixture increased the phosphorylation of IRS1 compared to the C group, as well as increased the phosphorylation of PI3K. In addition, AKT was activated and converted to its phosphorylated form, and the expression of GLUT4 increased by more than two-fold relative to the C group, thereby increasing the influx of glucose into cells to suppress lipogenesis induction. In addition, although additional studies are needed regarding insulin resistance, these results are considered to have potential as substances capable of controlling blood sugar by suppressing insulin resistance. In the lipogenesis mechanism, SREBP1c regulates FA synthesis and activates lipogenesis-related factors, including ACC and FAS [37]. ACC has generally been described in previous research as the rate-limiting enzyme system in de novo FA synthesis [38]. ACC is an enzyme that is responsible for the production of malonyl-CoA, which is the intermediate substrate required for chain extension by FAS, the multifunctional enzyme [39]. In addition, SREBP1c can stimulate the ligand for the nuclear receptor and activate PPARy transcription [40; 41]. AMPK acts as a sensor of cellular energy that regulates lipid metabolism, including anabolism and catabolism. Activated AMPK can inhibit lipogenesis by down-regulating SREBP1c protein expression [42; 43]. In addition, LPL secreted from adipocytes is involved in FA synthesis and lipoprotein metabolism [44]. In this cell model for inducing differentiation with an adipogenic cocktail, the activity of AMPK decreased and the expression of SREBP1c increased. In addition, the activity of ACC was inhibited and the FAS, LPL, and FA levels increased. The IGBP 2:1 mixture induced the reduction of SREBP1c by converting AMPK to the active type compared to the C group. In addition, treatment with the IGBP 2:1 mixture led to the expression of the active form of ACC, induced reductions in the FAS and LPL expression levels, and decreased the adipocyte FA level in a dose-dependent manner. These results affected reductions in lipid accumulation and TG content and led to increased glycerol release from the adipocytes (Figure 6). We expect that the anti-obesity activity of the IGBP mixture was due to ellagic acid and saponarin. Ellagic acid and saponarin have been found to be detected in the component analysis of the IGBP mixture (data not shown), and this result requires a little further validation and is expected to be active in animal studies as well.