MAFLD and impaired bone formation in children: association with reduced serum LCAT.

Purpose: To evaluate bone metabolism indicators and serum lecithin-cholesterol acyltransferase (LCAT) levels in children with metabolic dysfunction-associated fatty liver disease (MAFLD), and to explore their interrelationship. Patients and Methods: This study enrolled 127 children aged 6-14 years, classified into control (n = 42), obesity without hepatic steatosis (n = 41), and MAFLD (n = 44) groups. All participants underwent clinical evaluation, laboratory testing, and liver ultrasonography. Serum LCAT was quantified by enzyme-linked immunosorbent assay (ELISA). Bone turnover markers, including procollagen type I N-terminal propeptide (PINP), β-C-terminal telopeptide of type I collagen (β-CTX), and 25-hydroxyvitamin D [25-(OH) D], were measured via electrochemiluminescence. Independent risk factors for impaired bone formation were analyzed using multivariable ordinal logistic regression. Results: Serum LCAT concentrations were highest in controls (58.27 ± 4.43 mg/L), followed by obesity without hepatic steatosis (46.13 ± 3.37 mg/L), and lowest in the MAFLD group (40.71 ± 3.44 mg/L) ( Conclusion: MAFLD was independently associated with lower PINP status in children. Reduced serum LCAT levels were associated with MAFLD and unfavorable bone formation status but were not independently associated with PINP grade after multivariable adjustment. LCAT may therefore represent an associated biomarker within the liver-bone axis, requiring validation through prospective studies, formal mediation analyses, and mechanistic experiments.