## 4 Discussion  
HFD causes obesity in animals such as mice and is directly associated with type II diabetes, which is characterized by symptoms such as hyperglycemia, insulin resistance, obesity, renal degeneration, and hyperlipidemia [5; 12]. In all fSFP dose groups, including 250 mg/kg metformin, there was a decrease in BW over the entire 84-day drug test compared to the HFD control group. Obesity is the most common consequence, and histological studies have shown that it causes adipocyte hypertrophy [5; 12; 13; 22]. In addition to directly affecting adipose tissue, energy storage and endocrine systems, it can also release adipokines. According to [PERSON] et al. [31] and [PERSON] et al. [12; 13], changes in adipokine secretion can lead to complex diseases, including obesity and insulin resistance. The results of this study were that the fSFP group showed significant adipogenesis and adipocyte hypertrophy inhibition effects at all three doses compared with the HFD control group. It is known that when obesity occurs, the pancreas reduces the number of zymogen granules [32]. Histopathological, all three doses of fSFP groups increased zymogen granules in the exocrine pancreas; it indicates that this anti-obese effect may be through the production of fat digestive enzymes. As type II diabetes progresses, insulin resistance often leads to increased serum insulin and HbA1c levels [21]. Furthermore, to sustain glycemic equilibrium, chronic exposure to HFD leads to an increase in the quantity and proliferation of pancreatic cells, including both insulin- and glucagon-secreting cells, as well as a rise in the ratio of insulin/glucagon-producing cells [33]. Blood glucose, blood insulin, and HbA1c levels, as well as histological and immunohistochemical changes in the pancreatic endocrine region, decreased in all three doses of the fSFP groups; this reveals the effects of pancreatic endocrine function. The hypolipidic effect of the candidate increases the level of low lipoprotein, lower cholesterol and fat (triglycerides). As diabetes worsens, obesity and hepatocyte degradation lead to increased levels of AST, ALT, ALP, LDH, and GGT in the blood, known as the induction of NAFLD [34]. Moreover, fibrosis and hepatocellular damage from abnormal glycolysis can further deteriorate the liver [34]. The results of this study are that the fSFP-administered group showed anti-hyperlipidemic activity at all three doses, which reduced NAFLD in HFD-fed mice. Diabetic nephropathy is characterized by high blood BUN and creatinine levels and occurs when the diabetic condition progresses to glomerular atrophy and fibrosis, inflammatory cell infiltration, and tubular necrosis [35]. The effects of diabetic nephropathy were dose-dependently reduced in all three doses of the fSFP group, indicating an effect on diabetic nephropathy. It is also known that the development of various types of diabetes is directly related to cellular damage caused by oxidative stress [36]. Many free radicals are produced in diabetes due to strong oxidative stress and inhibition of endogenous antioxidants [37]. In this study, lipid peroxidation, which is associated with interference with antioxidant defense systems, was reduced in the three-dose fSFP group. In rats fed with HFD, it has been shown to exhibit decreased glucose-degrading enzyme and increased glucose-synthesizing enzyme, which often leads to a hyperglycnic state [21]. In addition, fSFP significantly and dose-dependently inhibited glucose metabolism enzymes in the liver. AMPK is now recognized as one of the most important cellular factors regulating blood sugar and fat metabolism by promoting fat oxidation and inhibiting fat synthesis and glucose production in the liver and adipose tissue [7]. Therefore, it is important to monitor the expression of this AMPK gene and AMPK signaling pathway-related proteins in the liver and adipose tissue. Additionally, PPARs are known to play a role in lipid oxidation and lipid synthesis [8; 11].