Jiangsu Key Laboratory of Druggability of Biopharmaceuticals, School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009，China.
Jiangsu Key Laboratory of Druggability of Biopharmaceuticals, School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009，China.
Life Sci. 2020 Jul 15;253:117677. doi: 10.1016/j.lfs.2020.117677. Epub 2020 Apr 17.
Impaired vascularization of adipose tissue leads to local hypoxia and results in chronic inflammation and obesity-related metabolic disorders. We have recently constructed an engineered protein named tPep-VEGF-B by bridging vascular endothelial growth factor (VEGF-B) with an adipose-targeted peptide. Here, we reported tPep-VEGF-B diminishes obesity and alleviates metabolic syndrome. High fat diet (HFD) treated mice had reduced adipose vascular density and showed adipose hypoxia and metabolic complications. In contrast, the treatment of tPep-VEGF-B repressed HFD-induced body weight gain, which led to increased adipose vasculature and reduced hypoxia. This treatment also alleviated obesity associated hyperlipidemia and fatty liver disease. This study provided a leading molecule for the treatment of type 2 diabetes and other metabolic diseases. It also provided experimental support for the theory that modulation of angiogenesis plays a key role in the treatment of metabolic diseases.
脂肪组织血管生成受损会导致局部缺氧，进而引发慢性炎症和与肥胖相关的代谢紊乱。我们最近构建了一种名为 tPep-VEGF-B 的工程蛋白，该蛋白通过将血管内皮生长因子 (VEGF-B) 与脂肪靶向肽连接起来。研究表明，tPep-VEGF-B 可减轻肥胖并缓解代谢综合征。高脂肪饮食 (HFD) 处理的小鼠脂肪血管密度降低，并表现出脂肪缺氧和代谢并发症。相比之下，tPep-VEGF-B 的治疗抑制了 HFD 诱导的体重增加，从而增加了脂肪血管生成并减少了缺氧。这种治疗还缓解了肥胖相关的高血脂和脂肪肝疾病。本研究为治疗 2 型糖尿病和其他代谢疾病提供了一种先导分子。它还为血管生成调节在治疗代谢疾病中发挥关键作用的理论提供了实验支持。
