Sedentary Behavior as a Risk Factor for Liver Fibrosis Development in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Cross-Sectional Study.
Аннотация
Background
Metabolic dysfunction-associated fatty liver disease (MASLD) affects nearly 20% of the Italian population, with an annual economic burden of € 7.94 billion on the National Health Service, largely due to advanced liver disease and metabolic comorbidities. Progressive liver fibrosis remains the strongest predictor of adverse outcomes. Early diagnosis is crucial, as fibrosis is potentially reversible in its early stages. Sedentary behavior (SB) is one of many modifiable risk factors for several chronic diseases; however, most evidence is based on self-reported data. This study investigates the association between objectively measured daily energy expenditure and liver stiffness in adults with MASLD.
Methods
We conducted a cross-sectional analysis of 104 adults (18-65 years) with obesity and moderate-to-severe steatosis (CAP ≥ 248 dB/m) from the Obesity-AF study. Daily energy expenditure (METs/day) was assessed via 7-day wrist-worn actigraphy. Liver stiffness (LSM, kPa) was measured non-invasively using transient elastography (FibroScan®).
Results
Lower daily energy expenditure was independently associated with higher liver stiffness. Each 1-MET increase correlated with a -1.239 kPa reduction in LSM (95% CI: -2.012, -0.466; p = 0.002). Sedentary individuals (≤1.5 METs) exhibited significantly higher LSM (+0.73 kPa, p = 0.03) versus non-sedentary peers, even after full adjustment. Findings were robust across sensitivity analyses.
Conclusions
Our study shows that SB, objectively measured by actigraphy, is independently associated with increased liver stiffness in patients with MASLD and obesity. Reducing sedentary time may represent a simple, low-cost, and scalable strategy to mitigate fibrosis progression. However, given the cross-sectional design and the specificity of our sample, longitudinal studies are needed to confirm the causal role of SB and to evaluate the effectiveness of targeted interventions in broader MASLD populations.
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