Commentary
A growing body of evidence places skeletal muscle and the muscle-liver axis at the center of the NAFLD pathogenic cascade. Skeletal muscle is implicated via its impact on insulin resistance and systemic inflammation.
Population-based studies suggest that sarcopenia is an effect-modifier across the NAFLD spectrum and is tightly linked to an increased risk of non-alcoholic fatty liver, NASH, and advanced liver fibrosis, independently of obesity and insulin resistance. Conversely, longitudinal studies suggest that increases in skeletal muscle mass over time may both reduce the incidence of NAFLD and improve preexisting NAFLD. Similarly, adverse muscle composition, comprising both low muscle volume and myosteatosis, is highly prevalent in patients with NAFLD. In their review, MV Chakravarthy et al. discuss key pathophysiological processes driving sarcopenia in NAFLD.
