The burden of NAFLD is increasing due to the global obesity epidemic, affecting approximately one-third of the population in the Western world (Friedman et al., 2018). The development of NAFLD is strongly associated with disorders in liver fat metabolism, in which PPARα plays a crucial role in maintaining energy homeostasis. PPARα regulates genes that control the uptake, oxidation, and hydrolysis of fatty acids and triglycerides in the liver (Bi et al., 2014). As a result, persistent PPARα activators are used in the clinical treatment of NAFLD to promote hepatic oxidation of peroxisome and mitochondrial fatty acids (Huang et al., 2012; Rotman and Sanyal, 2017).

The liver is a crucial organ that plays a role in regulating glucose and lipid metabolism, as well as maintaining systemic metabolic balance by interacting with other organs (Ye et al., 2017). The liver is a crucial organ that plays a role in regulating glucose and lipid metabolism, as well as maintaining systemic metabolic balance by interacting with other organs (Azzu et al., 2020). FGF21, an important cytokine produced by the liver, has diverse metabolic effects in various organs such as adipose tissue and skeletal muscle, which help combat obesity and diabetes (Flippo and Potthoff, 2021). The expression of the FGF21 gene in the liver is regulated by PPARα, with a PPARα response element present in the promoter of the human and mouse FGF21 genes (Lee et al., 2022). FGF21 has pharmacological properties that lead to positive metabolic effects, including the promotion of adipose tissue browning and energy expenditure, as well as improvements in glucose availability and insulin sensitivity (Flippo and Potthoff, 2021; Sun et al., 2021).

Adipose tissue can be categorized into two types: white adipose tissue (WAT) and brown adipose tissue (BAT). WAT primarily functions as an energy storage site, whereas BAT plays a crucial role in adaptive thermogenesis by utilizing energy (Rosen and Spiegelman, 2014). The thermogenic properties of BAT are attributed to its abundant mitochondria and high expression of UCP1, which is located in the inner mitochondrial membrane, and UCP1 facilitates adaptive thermogenesis by converting energy into heat (Betz and Enerback, 2018). In animal models, certain cytokines and compounds have demonstrated the ability to combat obesity by promoting adipocyte browning (Fisher et al., 2012; Nie et al., 2018). As a result, the investigation and creation of small molecular compounds that encourage browning have emerged as a crucial avenue for addressing obesity and metabolic disorders.

Magnolia officinalis is a plant species that is indigenous to Asia. Its main active component is the Magnolia officinalis extract, which contains Magnolol and Honokiol. It has been utilized as a traditional nutrient for centuries (Szalabska-Rapala et al., 2021; Tse et al., 2007). In a mouse model of obesity, it was discovered that Magnolol and Honokiol have anti-inflammatory properties (Suh et al., 2017), which reduce body weight gain by white adipose tissue (Choi et al., 2009). Additionally, they inhibit the development of diabetes (Alonso-Castro et al., 2011) and the accumulation of body fat (Ding et al., 2019). In vitro, Magnolol has been shown to contribute to the browning of 3T3-L1 adipocytes, enhance lipolysis and thermogenesis, and suppress oxidative stress and lipogenesis (Parray et al., 2018). Honokiol, on the other hand, plays an important modulatory role in adipocytes by inducing browning and apoptosis in 3T3-L1 adipocytes, as well as inhibiting apoptosis in HIB1B brown adipocytes (Lone and Yun, 2017).