## 1 Introduction  
Obesity serves as a root cause for various metabolic disorders, including hypertension, heart disease, and type II diabetes [1]. In the presence of obesity, adipocytes release diverse adipokines influencing both adipocyte and non-adipocyte metabolism, thereby triggering chronic inflammation and associated metabolic ailments such as insulin resistance [2]. Typically, adipocytes function to store lipids for long-term energy use in individuals with obesity. Consumption of a high-fat diet induces triglyceride (TG) accumulation in multiple tissues, heightens lipolysis, elevates circulating fatty acids, and induces insulin resistance in adipocytes. Consequently, excess fat is deposited in non-adipose tissues like the liver and muscles. The augmented binding and transport of fatty acids increase their uptake in non-adipocytes, particularly muscle cells, negatively impacting insulin-mediated glucose metabolism in cases of adipocyte insulin resistance. This lipotoxic process, due to prolonged exposure to fatty acids, diminishes insulin secretion in the pancreas [3]. TG formation in hepatocytes can lead to non-alcoholic fatty liver disease (NAFLD), characterized by he hepatocyte fat accumulation, steatohepatitisitis, and eventual hepatocyte necrosis and fibrosis, particularly affecting carbohydrate metabolism [4]. Research involving a high-fat diet (HFD) suggests that obese and hyperglycmic animal models can assist in evaluating the efficacy of functional foods to prevent diseases like NAFLD and metabolic syndrome [5]. Hence, the present study adopted a mouse model fed a 45% kcal high-fat diet to investigate the pharmacological action of fSFP in addressing metabolic syndrome, encompassing obesity. Peroxisome proliferatorator-activated receptor (PPAR) and 5\({}^{\prime}\) adenosine monophosphate-activated protein kinase (AMPK) are two representative cell-regulating factors that are crucial for biological fat synthesis [6; 7; 8]. The onset of inflammation and obesity-induced NAFLD is implied by a decline in AMPK activity [9; 10]. According to research by [PERSON] et al. [8] and [PERSON] et al. [11], PPAR is known to play a role in both lipid oxidation and lipid synthesis. PPAR and PPAR\(\alpha\) are both known to have a role in lipid oxidation and lipid synthesis, respectively. Efforts are underway to formulate glucosidase inhibitors and potent antioxidants with minimal adverse effects. These developments are crucial for effectively managing oxidative stress, recently identified as a key factor in the pathogenesis of diabetes and its complications. Concurrently, maintaining optimal glycemic control is increasingly recognized as a pivotal strategy in diabetes treatment [5; 12; 13]. As an example of an oral biguanide-based anti-diabetic medication, metformin is well-known for activating AMPK [14]. Metformin was used as the positive control group in this investigation. The fruit of _Schisandra chinensis_ (Turcz.) Baill., Schizandrae fructus, has five distinct flavors: sweet, sour, astringent, spicy, and salty. It also contains a significant amount of phenolic compounds, which have been linked to a number of pharmacological effects, including anti-inflammatory and antioxidant effects [15; 16]. Asian traditional medicine has employed _Schisandra chinensis_[17]. It is now known from a recent study that Schisandra chinensis, either alone or in combination with grape seed extract, has excellent anti-obesity and anti-diabetic benefits. It also boosts energy metabolism by increasing PGC-1 expression, which leads to an improvement in muscle strength [18]. In addition, it has been reported that _Schisandra chinensis_ pomace displays pharmacological action that is comparable to that of _Schisandra chinensis_[19; 20]. Consequently, efforts are being made to take steps to develop alternative medicines made from natural ingredients that have few adverse effects and are more potent.