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Adipose-inflammatory factor profiles in children with metabolically healthy obesity and their correlation with NAFLD
Jing Li1, Hongyun Shi1, Qiaoheng Xie1
1The Second Affiliated Hospital, Department of Pediatrics, Hengyang Medical School, University of South China, Hengyang, China.
Insights
Metabolically healthy obese (MHO) children show altered adipose-inflammatory factors, increasing non-alcoholic fatty liver disease (NAFLD) risk. These factors, including adiponectin and leptin, can identify metabolic health status and predict NAFLD severity in MHO children.
Area of Science:
- Pediatric Endocrinology
- Metabolic Syndrome
- Adipose Tissue Biology
Background:
- Obesity in children is categorized into metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO).
- Adipose tissue dysfunction and inflammation are implicated in metabolic complications of obesity, including non-alcoholic fatty liver disease (NAFLD).
- Understanding adipose-inflammatory factor profiles can differentiate obese phenotypes and predict NAFLD risk.
Purpose of the Study:
- To compare adipose-inflammatory factor profiles between MHO and MUO children.
- To assess the association of these factors with NAFLD severity in MHO children.
- To evaluate the diagnostic efficacy of these factors in distinguishing metabolic phenotypes.
Main Methods:
- Retrospective study of 500 obese children (MHO, MUO) and 162 metabolically healthy lean (MHL) controls.
- Measurement of anthropometric, metabolic parameters, and serum levels of key adipose-inflammatory factors (adiponectin, leptin, resistin, RBP-4, PGRN, TNF-α, IL-6, CCL2).
- ROC curve analysis for diagnostic efficacy; Spearman's correlation for associations with NAFLD activity score (NAS) and steatosis, activity, and fibrosis (SAF) score.
Main Results:
- Adipose-inflammatory factors (leptin, resistin, RBP-4, PGRN, TNF-α, IL-6, CCL2) were elevated in MHO and further in MUO compared to MHL; adiponectin showed an inverse trend (P < 0.05).
- These factors showed good to excellent diagnostic value for distinguishing MHL from obese phenotypes and moderate value for differentiating MHO from MUO (AUCs: 0.695-0.894 and 0.636-0.740, respectively).
- NAFLD prevalence was higher in MUO (46.15%) than MHO (29.01%) (P < 0.001). In MHO with NAFLD, adiponectin negatively correlated with NAS and SAF score, while other factors positively correlated (r = 0.468-0.681, P < 0.001).
Conclusions:
- MHO children exhibit adipose-inflammatory factor dysregulation and significant NAFLD risk.
- Adiponectin and leptin effectively discriminate metabolic phenotypes and correlate with liver injury severity in MHO children.
- These factors hold potential as early biomarkers and therapeutic targets for obesity-related liver disease.
Objective:
To compare adipose-inflammatory factor profiles between children with metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO), and analyze their associations with non-alcoholic fatty liver disease (NAFLD) severity in MHO.
Methods:
This retrospective study included 500 obese children (162 MHO, 338 MUO) and 162 metabolically healthy lean (MHL) controls. Anthropometric, metabolic parameters, and serum levels of key adipose-inflammatory factors (including adiponectin, leptin, resistin, RBP-4, PGRN, TNF-α, IL-6, and CCL2) were compared. ROC curve analysis was used to evaluate diagnostic efficacy of adipose-inflammatory factors for differentiating phenotypes. NAFLD prevalence was assessed, and relationships of adipose-inflammatory factors with NAFLD activity score (NAS) and steatosis, activity, and fibrosis (SAF) score in MHO children with NAFLD were analyzed by Spearman's correlation analysis.
Results:
Metabolic parameters and adipose-inflammatory factor levels (leptin, resistin, RBP-4, PGRN, TNF-α, IL-6, CCL2) were significantly higher in MHO than MHL, and further elevated in MUO, while adiponectin showed an inverse trend (all P < 0.05). These factors demonstrated good to excellent diagnostic value for distinguishing MHL from both obese phenotypes (AUC range: 0.695-0.894), and moderate value for distinguishing MHO from MUO (AUC range: 0.636-0.740; all P < 0.001). NAFLD prevalence was 29.01% in MHO vs. 46.15% in MUO (P < 0.001). In MHO children with NAFLD, adiponectin levels correlated negatively with NAS and SAF score (r = -0.668, -0.641), whereas all other factors showed positive correlations (r = 0.468-0.681, all P < 0.001).
Conclusion:
MHO children exhibit dysregulation of adipose-inflammatory factors and a considerable risk for NAFLD. These factors, especially adiponectin and leptin, effectively discriminate metabolic phenotypes and correlate with liver injury severity in MHO, suggesting their potential utility as early biomarkers and therapeutic targets.
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