## 4 Discussion  
Triglycerides are fats consisting of three fatty acids covalently bonded to a glycerol molecule and are the primary form of lipids in the liver tissue. Hypertriglyceridemia, which is related to excess accumulation of non-esterified fatty acids and cholesterol in the liver tissue, may result in hepatic steatosis, also known as NAFLD [23]. It was shown in this study, involving a rat model and Fr-induced HepG2 cells, that an HFrD caused hypertriglyceridemia, triggered hepatic TG accumulation, and amplified the expression of ChREBP and SREBPP-1 and their target enzymes HMGCR and FAS on molecular lipid metabolism markers. Fructose is sweeter and cheaper than sucrose and is widely used in the food industry. Every day, we unknowingly consume food items that contain high-fructose corn syrup, such as beverages, dairy products, and baking products. Regular fructose intake contributes to the development of lipid disorders, oxidative stress, and mild chronic inflammation, which are directly associated with obesity, NAFLD, and cardiovascular diseases [24]. This concern is supported by observations in human and rodent epidemiological studies that HFrD induces hepatic intrahepatocellular lipids, hepatic DNL, and abdominal aortic thickness, and increases hepatic insulin resistance [25; 26; 27]. Furthermore, consistent with our data, several studies have reported that HFrD-fed rats have increased hepatic levels of upstream regulators of DNL, such as SREBPP-1, ChREBP, key lipogenic enzymes, and pro-inflammatory cytokines [28; 29; 30; 31; 32]. ChREBP is a transcriptional operator of lipid and glucose metabolism, changing surplus carbohydrates into triglycerides [24]. The liver-specific inhibition of ChREBP aggravates insulin resistance, hepatic steatosis, and hypertriglyceridemia, followed by the downregulation of hepatic expression of gluconeogenesis and lipogenic genes in leptin-deficient mice [33; 34]. HFrD triggers ChREBP, which acts synergistically with SREBPP-1 to amplify lipogenic gene expressions [35]. SREBPP-1 is stimulated by insulin [36]. SREBPP-1 mediates the long-term regulation of lipid and glucose homeostasis by insulin; it alone does not appear to fully describe the stimulation of lipogenic and glycolytic gene expression in reaction to a carbohydrate diet [37]. In this study, an HFrD increased the levels of inflammatory cytokine TNF-\(\alpha\) and the oxidative stress protein iNOS in the hepatic tissue and HepG2 cells. Consistent with our data, previous studies have shown that HfrD causes a significant increase in oxidative stress markers (lipid peroxidation) such as iNOS, active cytokines such as TNF-\(\alpha\), and neutrophil infiltration in the liver, indicating an inflammatory response [38]. Moreover, some studies have reported that even short-term fructose feeding induces oxidative stress and inflammation in the hippocampus [39; 40]. Lipotoxicity caused by the excessive accumulation of hepatic lipids can lead to inflammation, fibrosis, and pathological angiogenesis [41]. EPK administration mitigated induced hypertriglyceridemia and hepatic steatosis. In addition, EPK downregulated the expression of lipogenesis factors, pro-inflammatory cytokine TNF-\(\alpha\), and iNOS. Our previous study demonstrated that EPK exerts anti-obesity effects in 3T3-L1 adipocytes and in high-fat-diet-induced obese rats [17]. Consistent with the present data, despite differences in the experimental model, EPK decreased lipid accumulation, TG levels, and SREBPP-1, HMGCR, and FAS expression in the differentiated 3T3-L1 cells and high-fat-diet animal model. Many researchers, including us, have reported that _P. koraiensis_ contains \(\alpha\)-pinene, camphene, borneol, D-limonene, lambertianic acid, bicyclo-hept-3-ene, \(\beta\)-pinene, 3-carene, fencyl alcohol, and \(\beta\)-phellandrene. It has been reported that D-limonene has anti-inflammatory properties [42]. Camphene has also been shown to have hypolipidemic effects in hyperlipidic rats [43].