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        <datestamp>2026-09-25T05:17:32Z</datestamp>
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          <dc:title>Table 1_MAFLD and impaired bone formation in children: association with reduced serum LCAT.docx</dc:title>
          <dc:creator>Lingyan Zhu (519291)</dc:creator>
          <dc:creator>Lin Xu (94491)</dc:creator>
          <dc:creator>Lanshu Yang (24595602)</dc:creator>
          <dc:creator>Baolan Sun (4569730)</dc:creator>
          <dc:creator>Weixia Yang (6250343)</dc:creator>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>pediatrics</dc:subject>
          <dc:subject>obesity</dc:subject>
          <dc:subject>MAFLD</dc:subject>
          <dc:subject>bone metabolism</dc:subject>
          <dc:subject>LCAT</dc:subject>
          <dc:subject>liver-bone axis</dc:subject>
          <dc:description>Purpose&lt;p&gt;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.&lt;/p&gt;Patients and Methods&lt;p&gt;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.&lt;/p&gt;Results&lt;p&gt;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) (P &lt; 0.001). The proportion of children with PINP below the 25th percentile was significantly greater in the MAFLD group (88.64%) than in obesity (48.78%) and control groups (35.71%) (P &lt; 0.001). Significant intergroup differences were observed for 25-(OH) D, PINP values, PINP grade, and PINP/β-CTX ratio; PINP grade distribution differed among groups (P &lt; 0.001), whereas β-CTX grade did not. Spearman analysis revealed significant correlations of LCAT with HDL-C, AST, ALT, fatty liver status, 25-(OH) D, and PINP grade (all P &lt; 0.001). Multivariable ordinal logistic regression identified MAFLD (OR = 4.74, 95% CI: 1.41–15.99, P = 0.012) and older age (OR = 1.38, 95% CI: 1.08–1.75, P = 0.009) as independent factors associated with lower PINP grade, whereas LCAT was not independently associated with PINP grade.&lt;/p&gt;Conclusion&lt;p&gt;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.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-25T05:17:32Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fcell.2026.1902360.s001</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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