SERUM LncRNA SNHG16: A Biomarker for Diagnosing Childhood Obesity and Predicting Its Progression to Metabolic Syndrome

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Purpose Obesity is a major risk factor for metabolic syndrome (MS) in children. This study explores the expression and clinical significance of long non-coding RNA SNHG16 (SNHG16) in childhood obesity and its complications with MS (obesity-MS). Patients and methods Healthy controls and obese children (categorized as those with simple obesity or obesity-MS) were enrolled. Serum SNHG16 and miR-27a-3p levels were quantified by RT-qPCR. ROC curves evaluated SNHG16's diagnostic value for obesity. Logistic regression analysis identified potential risk factors for the development of obesity-MS. DLR assay and RIP assay confirmed the interaction between SNHG16 and miR-27a-3p. Bioinformatics was used to predict downstream genes of miR-27a-3p and, then GO and KEGG enrichment analysis identified the functions and signaling pathways of these genes. Results Serum SNHG16 levels were distinctly upregulated in obese children, especially those with obesity-MS. In contrast, miR-27a-3p expression showed the opposite trend. Additionally, SNHG16 was positively correlated with BMI in obese children. Serum SNHG16 exhibited 81.18% sensitivity and 76.47% specificity in distinguishing controls from obese individuals. Furthermore, serum SNHG16, BMI, HOMA-IR, and TG are potential risk factors for MS in obese children. Mechanistically, SNHG16 directly targets miR-27a-3p, and miR-27a-3p targets 65 genes prim

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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