## 1 Introduction  
Handgrip strength (HGS) is an indicator of muscle function [1], and current guidelines have emphasized the significance of HGS as the principal metric for sarcopenia diagnosis [2]. Among adult individuals, HGS is a recognized marker of frailty as well as a reflection of their present nutritional status [3, 4, 5, 6, 7]. Furthermore, the loss of muscle function predisposes older adults to an increased risk of several clinical conditions [8] and mortality [5, 9, 10, 11]. It is established that muscle strength surpasses skeletal muscle mass in its predictive capacity for adverse outcomes [9, 12]. For these reasons, evaluating muscle strength is gaining greater significance in both research and clinical environments, with the aim of enhancing the well-being of aging populations. Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disorder [13, 14]. NAFLD presents a significant public health challenge due to its global surge, attributable to the obesity epidemic [13, 15], and its growing role as a primary contributor to hepatocellular carcinoma (HCC) [16]. NAFLD is also a predictor of cardiovascular diseases and a greater mortality rate [17, 18, 19]. Interestingly, hepatic steatosis and sarcopenia, both linked to the subject'sdietary habits, may share common pathogenic mechanisms such as insulin resistance (IR), chronic low-grade inflammation, and decreased physical activity [20; 21; 22]. Additionally, molecules such as myostatin, insulin-like growth factor-1 (IGF-1), and sirutin 1 (SIRT 1) are implicated in this relationship. Myostatin, a myokine expressed in skeletal muscle that is a negative regulator of skeletal muscle growth in animals and human is significantly higher in adults with sarcopenia than in those without sarcopenia [23]. Preclinical studies have demonstrated that inhibition of myostatin increases muscle mass, improves insulin sensitivity, and protects against liver steatosis [24; 25]. A low level of IGF-1, a regulator of both hepatic glucose production and skeletal muscle cells, has been demonstrated in individuals with NAFLD [26] as well as sarcopenia [27]. SIRT1 is also linked to the spectrum of liver damage and muscle atrophy [28; 29]. SIRT1 plays important roles in regulating lipid metabolism, inflammation, and oxidative stress in the liver through deacetylating some transcriptional regulators against the progression of fatty liver diseases [28]. Hepatic oxidative stress aggravates liver damage and muscle wasting progression. Indeed, in subjects with NAFLD, muscular oxidative stress promotes protein degradation, cell apoptosis, and the development of muscle atrophy [30]. Activation of SIRT-1 attenuates hepatic steatosis and improves muscle atrophy in an animal model of non-alcoholic steatohepatitis [30]. Furthermore, recent findings have shown that sarcopenia and reduced appendicular muscle mass serve as indicators for the development of impaired fasting glucose and type 2 diabetes in older women [31], and that IR and inflammation may modulate the connection between HGS and the risk of NAFLD [32]. To date, some studies have evaluated the relationship between muscle function and NAFLD, but especially in Asian populations [32; 33; 34; 35; 36; 37; 38; 39]. However, only two Asian studies have investigated this relationship exclusively in adults aged \(\geq\)50 years [35; 37], who represent the most vulnerable population to sarcopenia and its consequences. Hence, extrapolating these results to non-Asian groups may be problematic due to differences in muscle strength among ethnicities [9]. To date, this relationship has only been evaluated in two studies involving Caucasians [40; 41]. In particular, the first study supports the relationship between sarcopenia (as defined in the skeletal muscle index) and NAFLD, assessed with ultrasound, in American Caucasians [40].