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Regulation of Appetite and Obesity · Journal article
Frontiers in Pediatrics · August 18, 2026
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This cross-sectional study of 98 children found no significant difference in serum phoenixin-14 between obese children with and without metabolic syndrome, either unadjusted (p=0.955) or after adjustment for age and Tanner stage (p=0.676). The finding does not support a discriminative role for phoenixin-14 in pediatric MetS, but the small sample and absence of healthy controls limit the ability to determine whether phoenixin is altered in pediatric obesity at all.
Cross-sectional study. Children and adolescents aged 7–18 years: 45 with metabolic syndrome (defined by modified IDF criteria) and 53 with obesity without metabolic syndrome.. Intervention: Measurement of serum phoenixin-14 by sandwich ELISA in two groups stratified by obesity and metabolic syndrome status.. Compared with: Obese children without metabolic syndrome versus obese children with metabolic syndrome.. n = 98. Not stated.
Serum phoenixin-14 unadjusted: MetS 519.75 ± 196.67 vs. obese 567.86 ± 368.40 pg/mL, p=0.955 Adjusted difference after GLM (n=95): −26.5 pg/mL (95% CI: −152.1 to 99.1), p=0.676 Adjusted means: MetS 529.1 pg/mL vs. obese 555.7 pg/mL
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This negative finding suggests phoenixin-14 is not a useful marker for discriminating metabolic syndrome status in obese children. However, the absence of a healthy control group means the role of phoenixin in obesity per se remains unknown, limiting clinical utility at present.
Small cross-sectional study with a null primary finding in a novel biomarker; design and execution are sound but the negative result in a limited sample does not yet establish absence of association.
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This negative finding suggests phoenixin-14 is not a useful marker for discriminating metabolic syndrome status in obese children. However, the absence of a healthy control group means the role of phoenixin in obesity per se remains unknown, limiting clinical utility at present.
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Background Phoenixin is a novel neuropeptide encoded by the SMIM20 gene, implicated in energy homeostasis and reproduction, but its role in pediatric metabolic syndrome remains unknown. Methods This cross-sectional study enrolled 98 children and adolescents aged 7–18 years [45 with Metabolic syndrome (MetS) and 53 with obesity without MetS]. MetS was defined by modified International Diabetes Federation criteria. Biochemical analyses included fasting glucose, lipid profile, and liver enzymes on a Beckman Coulter AU5800 analyzer; insulin, cortisol, adrenocorticotropic hormone (ACTH), thyroid, and reproductive hormones on a Roche Cobas e601 electrochemiluminescence immunoassay system; and HbA1c by high-performance liquid chromatography (Bio-Rad D10). Serum phoenixin-14 was quantified by sandwich ELISA (Bioassay Technology Laboratory Cat. No. E7481Hu; sensitivity 8.19 ng/L; intra-assay CV 6.8%, interassay CV 9.2%). Group comparisons were performed using Mann–Whitney U and chi-square tests; a general linear model (GLM) adjusting for age and Tanner stage assessed the independent effect of the MetS and obese groups on serum phoenixin-14. Results Serum phoenixin-14 did not differ between the MetS and obese groups (519.75 ± 196.67 vs. 567.86 ± 368.40 pg/mL; p = 0.955). After adjustment for age and Tanner stage by GLM ( n = 95), the difference remained non-significant (adjusted difference: −26.5 pg/mL, 95% CI: −152.1 to 99.1; p = 0.676; adjusted means: MetS 529.1 pg/mL vs. Obese 555.7 pg/mL). Tanner stage was a significant covariate ( B = 73.04, p = 0.009). Children with MetS were older (13.62 ± 2.51 vs. 12.19 ± 2.65 years; p = 0.010) and had higher median insulin (30.80 vs. 18.20 µIU/mL; p 0.001), higher triglycerides (172.04 ± 70.94 vs. 106.68 ± 39.27 mg/dL; p 0.001), lower high-density lipoprotein-cholesterol (38.56 ± 7.73 vs. 47.02 ± 9.99 mg/dL; p 0.001), and higher ACTH (28.86 ± 14.12 vs. 22.44 ± 11.86 pg/mL; p = 0.018). Conclusions In this cohort, serum phoenixin-14 did not differ between obese children with and without metabolic syndrome after adjusting for age and pubertal stage ( p = 0.676). These findings do not support a discriminative role for phoenixin-14 in pediatric MetS. Further studies including healthy normal-weight controls are needed to determine whether phoenixin-14 concentrations are altered in pediatric obesity.
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