## 3 Results
### ESETM Prevents Development of Obesity in HFD-Fed Obese Mice  
To determine the anti-obesity effect of ESETM in HFD-fed obese mice, we fed ICR mice with ND, HFD, or HFD supplemented with 83 mg kg\({}^{-1}\) day\({}^{-1}\) (HFD + ESETML), 150 mg kg\({}^{-1}\) day\({}^{-1}\) (HFD + ESETMM), or 250 mg kg\({}^{-1}\) day\({}^{-1}\) (HFD + ESETMH) ESETM or 100 mg kg\({}^{-1}\) day\({}^{-1}\) _G. cambogia_ (HFD + GC) for 7 weeks. Although the groups did not differ significantly in initial body weight, the final body weight differed between the groups. Compared with the ND group, significant weight gain in the HFD group suggests that HFD-induced obesity. ESETM treatment significantly reduced the weight gain in a dose-dependent manner (Figure 2a,b). No significant differences were observed in food intake between the HFD group and ESETM- and GC-treated groups. In comparison with the HFD treatment group, the ESETM and GC treatment groups showed a decrease in the food efficiency ratio in a dose-dependent manner. These results suggest that ESETM and GC did not reduce food intake but reduced food efficiency (Figure 2c,d).  
As shown in Table 2, we measured the weight of each organ by dissecting mice after 7 weeks of oral administration of test agents. The weights of the WAT and liver were significantly higher in the HFD group than in the ND group. However, ESETM-treated groups showed a concentration-dependent decrease in the weight of WAT and liver. There was no significant difference in the weight change in height. In addition, the weight of the spleen increased in the mouse group fed with only HFD but did not significantly differ between the control group and the groups treated with ESETM. Therefore, one may speculate that ESETM inhibits the accumulation of fats inside the organ.  
AST and ALT levels were measured to investigate hepatotoxicity, and the triglyceride, total cholesterol, HDL, and LDL levels were determined to investigate the blood lipid concentrations. Serum AST and ALT activities, which are widely used as indicators of liver injury, were higher in the HFD group than in the ND group but reduced after oral ESETM treatment [26]. Furthermore, ESETM-treated HFD-fed mice had lower serum concentrations of triglycerides, total cholesterol, and LDL-cholesterol, and higher concentrations of HDL-cholesterol than those fed with HFD alone. The results show that ESETM also regulates blood cholesterol levels (Table 3).  
\begin{table}
\begin{tabular}{c c c c c c c} \hline \hline \multirow{2}{*}{**Compound**} & **Regression** & **HFD** & **HFD + GC** & **HFD + ESETML** & **HFD + ESETMM** & **HFD + ESETMM** \\ \hline WAT (mg) & 843.17 \(\pm\) 86.08 \({}^{\rm{e}}\) & 2867.67 \(\pm\) 179.88 \({}^{\rm{a}}\) & 1487.87 \(\pm\) 134.10 \({}^{\rm{d}}\) & 2332.87 \(\pm\) 111.24 \({}^{\rm{b}}\) & 1996.90 \(\pm\) 211.67 \({}^{\rm{c}}\) & 1563.60 \(\pm\) 246.85 \({}^{\rm{d}}\) \\ Liver (mg) & 1126.50 \(\pm\) 63.01 \({}^{\rm{e}}\) & 2229.33 \(\pm\) 19.59 \({}^{\rm{a}}\) & 1298.13 \(\pm\) 9.97 \({}^{\rm{d}}\) & 1732.47 \(\pm\) 144.97 \({}^{\rm{b}}\) & 1586.93 \(\pm\) 97.93 \({}^{\rm{c}}\) & 1292.70 \(\pm\) 29.53 \({}^{\rm{d}}\) \\ Kidney (mg) & 549.73 \(\pm\) 1.16 \({}^{\rm{a}}\) & 542.07 \(\pm\) 71.05 \({}^{\rm{a}}\) & 559.03 \(\pm\) 17.76 \({}^{\rm{a}}\) & 552.10 \(\pm\) 38.06 \({}^{\rm{a}}\) & 575.60 \(\pm\) 33.08 \({}^{\rm{a}}\) & 569.57 \(\pm\) 21.29 \({}^{\rm{a}}\) \\ Spleen (mg) & 123.50 \(\pm\) 9.44 \({}^{\rm{b}}\) & 151.70 \(\pm\) 4.65 \({}^{\rm{a}}\) & 122.80 \(\pm\) 19.19 \({}^{\rm{b}}\) & 121.60 \(\pm\) 13.08 \({}^{\rm{b}}\) & 125.43 \(\pm\) 2.03 \({}^{\rm{b}}\) & 123.80 \(\pm\) 5.29 \({}^{\rm{b}}\) \\ \hline \hline \end{tabular}  
* The results are expressed as mean \(\pm\) SD (\(n=5\)). Different lower case letters above columns indicate statistical differences among groups at \(p<0.05\) by one-way ANOVA.  
\end{table}
Table 2: Oran weights in ICR mice with ESETM.