## 4 Discussion
Despite this accumulating evidence, the precise relationship between muscle health and metabolic disorders like NAFLD remains incompletely understood. Although our study did not directly assess the mechanisms underlying this relationship, we can nevertheless make some hypotheses. The role of IR, chronic inflammation, and decreased physical activity has already been demonstrated [20; 21; 22]. In fact, as IR and inflammation increase, the prevalence of NAFLD increases and muscle strength decreases [20; 21; 33; 36]. Therefore, sarcopenia itself may aggravate IR in non-obese and obese individuals [71]. Furthermore, [PERSON] et al. demonstrated that both non-obese and obese individuals exhibited a markedly higher prevalence of NAFLD in the presence of sarcopenia [34]. In particular, the prevalence of NAFLD was 9-30% in non-obese sarcopenia individuals and 4-14% in non-obese and non-sarcopenia patients, while the prevalence of NAFLD was 61-83% in obese sarcopenia and 50-72% in obese non-sarcopenia patients [34]. Hence, factors beyond insulin resistance and obesity may play a role in the connection between muscle tissue and the liver, including IGF-1, myostatin, and SIRT 1. In particular, a systematic review and meta-analysis revealed that individuals with NAFLD exhibit lower levels of IGF-1 when compared to healthy control subjects [26]. Nevertheless, IGF-1 is also present in skeletal muscles, where it promotes muscle growth and strength, mitigates degeneration, hinders inflammatory processes, and stimulates the regenerative capacity of satellite cells [72]. In addition, a recent study demonstrated that elderly individuals with sarcopenia exhibit lower IGF-1 levels compared to those without sarcopenia (98.53 \(\pm\) 28.45 vs. 136.41 \(\pm\) 48.95 ng/mL, \(p\) < 0.001) [27]. Information on serum myostatin levels in individuals with sarcopenia is somewhat limited. However, a connection exists between IGF-1 and myostatin under usual circumstances. IGF-1 acts to obstruct the myostatin pathway; indeed, when IGF-1 is suppressed, myostatin becomes overexpressed [73]. SIRT1 is linked to liver damage and muscle atrophy, regulating lipid metabolism and countering oxidative stress in the liver. It plays a crucial role in fatty liver disease and muscle health [28; 29]. All these mechanisms suggest a strong link between skeletal muscle and the liver and, consequently, between sarcopenia and NAFLD. However, it remains uncertain whether impaired muscle function and sarcopenia lead to NAFLD, if it's the other way around, or whether the relationship does not involve a causal link but rather simultaneous effects on both the liver and muscles. In our study, we also found in tertile I a serum level of AST lower than tertile III (tertile I with a lower rHGS and higher CAP score than participants in tertile III). This is not surprising because it has already been shown that some patients with NAFLD may have laboratory abnormalities such as high ALT and AST, whereas others may have normal transaminase levels [74]. There is consensus on the fact that NAFLD is diagnosed in clinical settings using ultrasound imaging (as a liver biopsy is not practically feasible). Nice guidelines recommend not using routine liver blood tests to rule out NAFLD but rather offering a liver ultrasound to test people for NAFLD (National Guideline Centre (UK)) [75]. Risk groups recommended for NAFLD screening are the American Association for the Study of Liver Diseases (AASLD) and Asian Pacific Association for the Study of the Liver (APASL), diabetics, and patients who are overweight/obesity with a family history of cirrhosis, moderate-to-high alcohol consumption, or metabolic syndrome [76; 77]. Despite having the disease, up to 50% of NAFLD patients can have normal ALT and AST levels [76; 78; 79]. Elastography can accurately diagnose liver steatosis, especially if the IQR is less than 30% of the median [80]. Our study does have certain limitations.