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首页> 外文期刊>The Journal of Nutritional Biochemistry >Involvement of serum vascular endothelial growth factor family members in the development of obesity in mice and humans
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Involvement of serum vascular endothelial growth factor family members in the development of obesity in mice and humans

机译：血清血管内皮生长因子家族成员参与小鼠和人类肥胖的发展

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Adipose tissue is highly vascularized implying that angiogenesis takes place in its expansion. The aim of this study was to compare the concentrations of members of the vascular endothelial growth factor (VEGF) family in obesity. Serum concentrations of VEGFs were analyzed in 15 lean (BMI 20.3+-2.5 kg/m2) and 24 obese (BMI 47.6+-5.9 kg/m2) volunteers. Obese patients showed significantly increased circulating VEGF-A (150+-104 vs. 296+-160 pg/ml; Pb.05), VEGF-B (2788+-1038 vs. 4609+-2202 arbitrary units; Pb.05) and VEGF-C (13 453+-5750 vs. 17 635+-5117 pg/ml; Pb.05) concentrations. Interestingly, levels of VEGF-D were reduced in obese individuals (538+-301 vs. 270+-122 pg/ml; Pb.01). In addition, VEGF-A significantly decreased after weight loss following Roux-en-Y gastric bypass (BMI from 46.0+-8.0 to 28.9+-4.2 kg/m2 Pb.0001 vs. initial) from 345+-229 to 290+-216 pg/ml (Pb.01). Moreover, in order to corroborate the human findings VEGF-A levels were analyzed during the expansion of adipose tissue in two dynamic models of murine obesity. Serum VEGF-A was significantly increased after 12 weeks on a high-fat diet (43.3+-9.0 vs. 29.7+-9.1 pg/ml; Pb.01) or in ob/ob mice (52.2+-18.0 vs. 29.2+-7.7 pg/ml; Pb.01) and was normalized after leptin replacement in the latter (32.4+-14.0 pg/ml; Pb.01 vs. untreated ob/ob). Our data indicates the involvement of these factors in the expansion of adipose tissue that takes place in obesity in relation to the need for increased vascularization, suggesting that manipulation of the VEGF system may represent a potential target for the pharmacological treatment of obesity.
机译：脂肪组织高度血管化，意味着血管发生在其扩张中。这项研究的目的是比较肥胖中血管内皮生长因子（VEGF）家族成员的浓度。在15名瘦弱者（BMI 20.3 + -2.5 kg / m2）和24名肥胖者（BMI 47.6 + -5.9 kg / m2）中分析了VEGF的血清浓度。肥胖患者显示循环VEGF-A显着增加（150 + -104 vs. 296 + -160 pg / ml; Pb.05），VEGF-B（2788 + -1038 vs. 4609 + -2202任意单位; Pb.05）和VEGF-C（13 453 + -5750对17 635 + -5117 pg / ml; Pb.05）浓度。有趣的是，肥胖个体的VEGF-D水平降低（538 + -301对270 + -122 pg / ml; Pb.01）。此外，Roux-en-Y胃旁路手术后体重减轻后VEGF-A显着降低（BMI从46.0 + -8.0降至28.9 + -4.2 kg / m2 Pb.0001与初始相比）从345 + -229降至290 +- 216 pg / ml（Pb.01）。此外，为了证实人类的发现，在两种小鼠肥胖症动态模型中，在脂肪组织扩张过程中分析了VEGF-A水平。高脂饮食（43.3 + -9.0 vs. 29.7 + -9.1 pg / ml; Pb.01）或ob / ob小鼠（52.2 + -18.0 vs. 29.2+）在12周后血清VEGF-A显着增加-7.7 pg / ml; Pb.01），并在后者中替代瘦素后归一化（32.4±-14.0 pg / ml; Pb.01与未处理的ob / ob）。我们的数据表明，与增加血管生成的需求相关，这些因素参与了肥胖发生的脂肪组织的扩张，这表明对VEGF系统的操纵可能代表了肥胖症药物治疗的潜在目标。

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