Darılmaz Samed Emre, Tugrul Aksakal Melike Zeynep, Ceylan Gozde, Kucukgergin Canan, Yetim Sahin Aylin, Bekpinar Seldag
Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Department of Pediatrics, Division of Adolescent Medicine, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Scand J Clin Lab Invest. 2025;85(4):263-268. doi: 10.1080/00365513.2025.2502947. Epub 2025 May 14.
This study aimed to investigate the effect of obesity on angiogenesis and its relationship with liver steatosis in obese children and adolescents. The study ıncluded 81 obese ın chıldren and 30 healthy controls. Obese subjects were subdıvıded by ultrasound ınto three groups: no steatosıs, grade 1 lıver steatosıs (NAFL), and grade 2 NAFL. Obese individuals, regardless of the presence of NAFL, exhibited significant insulin resistance ( < .01) compared to their lean counterparts. All obese subjects showed elevated serum ALT, wıth a sıgnıfıcantly greater ın those wıth NAFL. Marked dyslipidemia by decreased high-density lipoprotein (HDL) levels and elevated triglycerides, was observed in obese individuals with NAFL. The serum levels of angiopoietin-1 (Ang-1) and vascular endothelial growth factor-165b (VEGF165b) were measured as anti-angiogenic markers, while vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor-2 (FGF-2) and P-selectin were assessed as pro-angiogenic factors. Compared to normal-weight children (5558 ± 674 pg/mL), Ang-1 levels were significantly elevated in all obese subgroups (8861 ± 1026; 8105 ± 615; 7388 ± 924, respectıvely). However, no significant differences in Ang-1 levels were observed among the obese subgroups. Ang-1 and VEGF165b levels were significantly higher in insulin-resistant individuals (7575 ± 747 pg/mL and 293 ± 44.4 pg/mL, respectively) compared to insulin-sensitive subjects (6143 ± 557 pg/mL and 179 ± 31.4 pg/mL, respectively). These findings suggest that insulin resistance in obese children is associated with altered angiogenic signaling. However, no significant differences in the serum levels of angiogenic factors were observed between obese groups with and without NAFL.
本研究旨在调查肥胖对肥胖儿童和青少年血管生成的影响及其与肝脂肪变性的关系。该研究纳入了81名肥胖儿童和30名健康对照。通过超声将肥胖受试者分为三组：无脂肪变性、1级肝脂肪变性（NAFL）和2级NAFL。与瘦的同龄人相比，肥胖个体无论是否存在NAFL，均表现出显著的胰岛素抵抗（<0.01）。所有肥胖受试者的血清ALT均升高，NAFL患者升高更为显著。在患有NAFL的肥胖个体中观察到明显的血脂异常，即高密度脂蛋白（HDL）水平降低和甘油三酯升高。测量血清血管生成素-1（Ang-1）和血管内皮生长因子-165b（VEGF165b）水平作为抗血管生成标志物，同时评估血管内皮生长因子-A（VEGF-A）、成纤维细胞生长因子-2（FGF-2）和P-选择素作为促血管生成因子。与正常体重儿童（5558±674 pg/mL）相比，所有肥胖亚组的Ang-1水平均显著升高（分别为8861±1026；8105±615；7388±924）。然而，肥胖亚组之间未观察到Ang-1水平的显著差异。与胰岛素敏感受试者（分别为6143±557 pg/mL和179±31.4 pg/mL）相比，胰岛素抵抗个体的Ang-1和VEGF165b水平显著更高（分别为7575±747 pg/mL和293±44.4 pg/mL）。这些发现表明，肥胖儿童的胰岛素抵抗与血管生成信号改变有关。然而，在有和没有NAFL的肥胖组之间，血管生成因子的血清水平未观察到显著差异。
