Among the mechanisms involved in the NAFLD-induced sarcopenia is the increased proinflammatory status (by secretion of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and angiotensin-II (Ang-II) as part of renin-angiotensin system (RAS) pathway) and alteration in muscle protein metabolism (by secretion of myostatin and ammonium) (see Figure 3). Here, IL6 is linked to metabolic dysfunction-associated steatotic liver disease.