Hernández-DíazCouder Adrián, Paz-González Pablo J, Valdez-Garcia Maryori, Ramírez-Silva Claudia I, Avila-Soto Karol Iliana, Pérez-Bautista Araceli, Vazquez-Moreno Miguel, Nava-Cabrera Ana, Romero-Nava Rodrigo, Huang Fengyang, Cruz Miguel
Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico.
Nutrients. 2025 Aug 2;17(15):2546. doi: 10.3390/nu17152546.
Obesity and its complications have increased in both adults and children, with pediatric populations developing metabolic disorders at earlier ages. Long non-coding RNAs, particularly , are involved in obesity through regulation of lipogenic genes including , , , , and . However, data on expression in pediatric obesity are limited. This study evaluated , , and expression in PBMCs from children with obesity and their associations with added sugar intake and lipid metabolism genes.
In this cross-sectional study 71 children within the age range of 6 to 12 years were included (28 normal weight and 43 with obesity). Anthropometrical and clinical parameters and dietary added sugar consumption were analyzed. Real-time PCR was performed to assess , , , , , and gene expression in peripheral blood mononuclear cells.
The expression of , , , , , and was decreased in children with obesity. and showed sex-dependent expression in children without obesity, while additional sex-related differences were observed for , , , , and in children with obesity. was associated with the expression of , , , , and . In insulin-resistant (IR) children, , , , , and were reduced, while was increased. Added sugar intake negatively correlated with , , and .
The , , and expression was altered in children with obesity, showing sex- and IR-related differences. Added sugar intake correlated negatively with lipogenic gene expression.
肥胖及其并发症在成人和儿童中均有所增加,儿童群体在更早的年龄就出现代谢紊乱。长链非编码RNA,尤其是[具体名称未给出],通过调控包括[具体基因名称未给出]、[具体基因名称未给出]、[具体基因名称未给出]、[具体基因名称未给出]和[具体基因名称未给出]等脂肪生成基因参与肥胖过程。然而,关于[具体名称未给出]在儿童肥胖中表达的数据有限。本研究评估了肥胖儿童外周血单核细胞(PBMCs)中[具体名称未给出]、[具体名称未给出]和[具体名称未给出]的表达及其与添加糖摄入和脂质代谢基因的关联。
在这项横断面研究中,纳入了71名6至12岁的儿童(28名体重正常,43名肥胖)。分析了人体测量和临床参数以及饮食中添加糖的摄入量。采用实时聚合酶链反应(PCR)评估外周血单核细胞中[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]和[具体基因名称未给出]的基因表达。
肥胖儿童中[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]和[具体名称未给出]的表达降低。在体重正常的儿童中,[具体名称未给出]和[具体名称未给出]表现出性别依赖性表达,而在肥胖儿童中,观察到[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]和[具体名称未给出]存在其他与性别相关的差异。[具体名称未给出]与[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]和[具体名称未给出]的表达相关。在胰岛素抵抗(IR)儿童中,[具体名称未给出]、[具体名称未给出]、[具体名称未给出]、[具体名称未给出]和[具体名称未给出]降低,而[具体名称未给出]增加。添加糖摄入与[具体名称未给出]、[具体名称未给出]和[具体名称未给出]呈负相关。
肥胖儿童中[具体名称未给出]、[具体名称未给出]和[具体名称未给出]的表达发生改变,呈现出与性别和胰岛素抵抗相关的差异。添加糖摄入与脂肪生成基因表达呈负相关。