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Background <p>Early cardiovascular risk in children demands biomarkers linking adiposity to vascular injury. We examined whether serum FAM132A (Adipolin) associates with endothelial dysfunction markers in Chinese children with obesity.</p> Methods <p>In a STROBE-guided single-center case–control study (Sep 2023–Mar 2024), we enrolled 82 children with obesity and 50 age-matched normal-weight controls; all participants underwent clinical assessment and anthropometry, and serum FAM132A, adiponectin, leptin and endothelial markers VCAM-1, E-selectin and ESM-1 were measured by ELISA. Multiple linear regression tested independent associations with adjustment for age, sex, pubertal stage, HOMA-IR and leptin.</p> Results <p>Mean FAM132A was higher in the obesity group (0.97 ± 0.13 vs 0.79 ± 0.07 ng/ml, <i>p</i> &lt; 0.001) and correlated positively with BMI, SDS-BMI, WHR, ALT and the three endothelial markers. In fully adjusted models FAM132A independently predicted VCAM-1 (<i>β</i> = 1.110, <i>p</i> = 0.040), E-selectin (<i>β</i> = 1.210, <i>p</i> = 0.043) and ESM-1 (<i>β</i> = 1.257, <i>p</i> = 0.041); these associations persisted after accounting for insulin resistance and were independent of classic adipokines.</p> Conclusion <p>Serum FAM132A is paradoxically elevated in pediatric obesity and independently associated with endothelial activation, suggesting compensatory upregulation in early metabolic stress and potential utility as an early vascular injury biomarker and merits longitudinal validation.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Serum FAM132A elevated in obese Chinese children.</p> </ItemContent> <ItemContent> <p>FAM132A correlates with endothelial markers VCAM-1, E-selectin, and ESM-1.</p> </ItemContent> <ItemContent> <p>Associations independent of insulin resistance and classic adipokines.</p> </ItemContent> <ItemContent> <p>Suggests compensatory upregulation during early metabolic stress.</p> </ItemContent> <ItemContent> <p>Implication: FAM132A as early biomarker for pediatric vascular injury.</p> </ItemContent> </UnorderedList></p>

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Serum FAM132A/Adipolin correlates with endothelial dysfunction in children with obesity

  • 期刊论文

  • 发表日期：

    2026年6月23日

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  • Yan Jin,
  • Yi Ding,
  • Hua Li,
  • Biyao Lian,
  • Xiaokang Wu,
  • Ning Gao,
  • Wen Zhang,
  • Chunyan Yin

摘要

Background

Early cardiovascular risk in children demands biomarkers linking adiposity to vascular injury. We examined whether serum FAM132A (Adipolin) associates with endothelial dysfunction markers in Chinese children with obesity.

Methods

In a STROBE-guided single-center case–control study (Sep 2023–Mar 2024), we enrolled 82 children with obesity and 50 age-matched normal-weight controls; all participants underwent clinical assessment and anthropometry, and serum FAM132A, adiponectin, leptin and endothelial markers VCAM-1, E-selectin and ESM-1 were measured by ELISA. Multiple linear regression tested independent associations with adjustment for age, sex, pubertal stage, HOMA-IR and leptin.

Results

Mean FAM132A was higher in the obesity group (0.97 ± 0.13 vs 0.79 ± 0.07 ng/ml, p < 0.001) and correlated positively with BMI, SDS-BMI, WHR, ALT and the three endothelial markers. In fully adjusted models FAM132A independently predicted VCAM-1 (β = 1.110, p = 0.040), E-selectin (β = 1.210, p = 0.043) and ESM-1 (β = 1.257, p = 0.041); these associations persisted after accounting for insulin resistance and were independent of classic adipokines.

Conclusion

Serum FAM132A is paradoxically elevated in pediatric obesity and independently associated with endothelial activation, suggesting compensatory upregulation in early metabolic stress and potential utility as an early vascular injury biomarker and merits longitudinal validation.

Impact

Serum FAM132A elevated in obese Chinese children.

FAM132A correlates with endothelial markers VCAM-1, E-selectin, and ESM-1.

Associations independent of insulin resistance and classic adipokines.

Suggests compensatory upregulation during early metabolic stress.

Implication: FAM132A as early biomarker for pediatric vascular injury.