## 4 Discussion  
This study demonstrated the beneficial effects of FGK administration on metabolic syndrome and inflammation in HFD-induced NAFLD mice. Our results showed that FGK significantly reduced the levels of serum ALT, AST, TC, TG, and glucose, indicating its protective effects against NAFLD-related liver damage and metabolic dysfunction. Furthermore, FGK inhibited the expression of inflammatory factors through the SIRT1/AMPK pathway, which plays a central role in lipid metabolism, oxidative stress, and inflammation regulation. The SIRT1/AMPK pathway is known to play a crucial role in the occurrence of metabolic syndrome and inflammation related to NAFLD, as well as oxidative stress. The administration of a high-fat diet (HFD) with elevated fat content is a well-established model for inducing obesity and NAFLD in mice by providing a high-calorie intake [30]. In this study, HFD-fed mice exhibited insulin resistance (IR), as confirmed by our IPGTT analysis, and hepatic steatosis, as observed in H&E-stained liver sections. These findings align with previous studies demonstrating that the HFD induces metabolic dysfunction, including impaired glucose metabolism and lipid accumulation in the liver [31]. FGK administration, however, significantly improved glucose tolerance and reduced hepatic lesions, suggesting its potential to mitigate NAFLD progression. NAFLD development is closely linked to excessive lipid accumulation, which leads to mitochondrial dysfunction, hepatocyte apoptosis, and inflammatory response [30; 31]. Our results demonstrated that FGK administration reduced serum ALT and AST levels, indicating its hepatotoxicity effects in HFD-fed mice. This aligns with the proposed role of antioxidants and bioactive compounds in fermented foods, which have been reported to improve liver function [24]. Furthermore, similar to finding in other studies, FGK administration reduced serum TC and TG concentrations and improved lipid metabolism in NAFLD models. These effects are likely mediated through the inhibition of de novo lipogenesis (DNL), a process that contributes to TG accumulation and is considered a therapeutic target in metabolic disorders [31]. AMPK, a key regulator of lipid and glucose metabolism, has been highlighted in recent studies as a critical pathway for addressing metabolic disorders, including NAFLD [32; 33]. In this study, FGK activated the SIRT1/AMPK pathway, which is known to reduce lipid synthesis and promote fatty acid oxidation. This provides a mechanistic basis for the observed improvements in lipid metabolism and inflammation, further justifying FGK's potential as a therapeutic agent. AMPK is a key regulator of protein that plays important roles in aging, inflammation, oxidative stress, and lipid and glucose metabolism [34]. Its activation is crucial for mitigating hepatic steatosis in NAFLD, as it reduces lipid markers such as TG and LDL while promoting fatty acid oxidation [35]. Similarly, SIRT1 is a transcription factor known as the \"master regulator of metabolism\", playing a central role in lipid metabolism homeostasis by regulating processes such as lipid accumulation and maturation in hepatic lipid metabolism and inflammation [32; 36]. Together, SIRT1 and AMPK regulate lipid metabolism through mutual interaction, forming a vital axis in addressing metabolic disorders. Several studies have reported that activation of the SIRT1/AMPK pathway in mice with NAFLD is associated with the alleviation of hepatic steatosis, inhibition of oxidative stress, and protection against metabolic disorders [13; 37]. In our study, FGK administration activated and upregulated the SIRT1/AMPK pathway, as demonstrated by reduced hepatic steatosis and inflammation in HFD-fed mice. These findings suggest that FGK's bioactive compounds, enhanced through fermentation, may directly modulate this pathway to exert its protective effects against NAFLD.