Hu Junjie, Zheng Zufen, Liang Dakang, Zhang Yongjin, Chen Jiejing, Zhou Cuiyi, You Chuming, Liu Qiong
Department of General Pediatrics, Sihui People's Hospital, Sihui, 526200, People's Republic of China.
Department of Neonatal Pediatrics, Sihui People's Hospital, Sihui, 526200, People's Republic of China.
Diabetes Metab Syndr Obes. 2025 Jul 9;18:2305-2316. doi: 10.2147/DMSO.S513449. eCollection 2025.
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).
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.
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 primarily enriched in insulin response and the MAPK, Ras, and mTOR signaling pathways.
Elevated serum SNHG16 levels may serve as diagnostic biomarkers for obese children and predict obesity-MS. SNHG16 may also contribute to the progression of obesity and MS by targeting miR-27a-3p.
肥胖是儿童代谢综合征（MS）的主要危险因素。本研究探讨长链非编码RNA SNHG16（SNHG16）在儿童肥胖及其合并MS（肥胖-MS）中的表达及临床意义。
纳入健康对照者及肥胖儿童（分为单纯肥胖或肥胖-MS）。采用RT-qPCR定量检测血清SNHG16和miR-27a-3p水平。ROC曲线评估SNHG16对肥胖的诊断价值。Logistic回归分析确定肥胖-MS发生的潜在危险因素。DLR分析和RIP分析证实SNHG16与miR-27a-3p之间的相互作用。利用生物信息学预测miR-27a-3p的下游基因，然后通过GO和KEGG富集分析确定这些基因的功能和信号通路。
肥胖儿童血清SNHG16水平明显上调，尤其是肥胖-MS儿童。相比之下，miR-27a-3p表达呈相反趋势。此外，肥胖儿童中SNHG16与BMI呈正相关。血清SNHG16在区分对照组与肥胖个体时表现出81.18%的敏感性和76.47%的特异性。此外，血清SNHG16、BMI、HOMA-IR和TG是肥胖儿童发生MS的潜在危险因素。机制上，SNHG16直接靶向miR-27a-3p，miR-27a-3p靶向65个主要富集于胰岛素反应以及MAPK、Ras和mTOR信号通路的基因。
血清SNHG16水平升高可能作为肥胖儿童的诊断生物标志物并预测肥胖-MS。SNHG16也可能通过靶向miR-27a-3p促进肥胖和MS的进展。
