Balwierz Adriana, Polus Anna, Razny Urszula, Wator Lukasz, Dyduch Grzegorz, Tomaszewska Romana, Scherneck Stephan, Joost Hans, Dembinska-Kiec Aldona
Department of Clinical Biochemistry, Collegium Medicum, Jagiellonian University, Cracow, Poland.
Lipids Health Dis. 2009 Apr 6;8:13. doi: 10.1186/1476-511X-8-13.
Obesity and its complications lead to vascular injury, atherosclerosis, diabetes and pathological angiogenesis. One of the models to study the obesity and its entanglements is the New Zealand Obese mice model. Aim of this study was to check the effect of high fat diet on changes in biochemical parameters as well as on process of angiogenesis in NZO mice.
NZO mice were fed with standard (ST) or high fat (HF) diet for seven weeks. Body weight and serum biochemical parameters were monitored. The PECAM1 positive vessel-like structures immunostaining, as well as the gene expression of the matrigel penetrating cells by microarray (confirmed by real-time PCR method) were analyzed.
Mice fed with HF diet developed obesity. Number of newly created vessels with lumen was correlated with hyperglycemia and animal weight gain. The number of PECAM1 positive cells in matrigel tended to increase during HF diet. Microarray results revealed changes in gene expression (activation of the oxidative stress and insulin resistance, inhibition of apoptosis and cell differentiation), however without markers of endothelial cell network maturation.
Observed changes in the NZO mice on HF diet argue for the hyperglycemia related activation of angiogenesis, leading to the formation of pathological, immature network.
肥胖及其并发症会导致血管损伤、动脉粥样硬化、糖尿病和病理性血管生成。研究肥胖及其相关问题的模型之一是新西兰肥胖小鼠模型。本研究的目的是检测高脂饮食对新西兰肥胖小鼠生化参数变化以及血管生成过程的影响。
给新西兰肥胖小鼠喂食标准(ST)或高脂(HF)饮食七周。监测体重和血清生化参数。分析血小板内皮细胞黏附分子1(PECAM1)阳性血管样结构免疫染色以及通过微阵列检测基质胶穿透细胞的基因表达(通过实时聚合酶链反应方法确认)。
喂食高脂饮食的小鼠出现肥胖。新形成的有腔血管数量与高血糖和动物体重增加相关。在高脂饮食期间,基质胶中PECAM1阳性细胞数量有增加趋势。微阵列结果显示基因表达发生变化(氧化应激和胰岛素抵抗激活,细胞凋亡和细胞分化受到抑制),但没有内皮细胞网络成熟的标志物。
在高脂饮食的新西兰肥胖小鼠中观察到的变化表明,高血糖相关的血管生成激活导致了病理性、不成熟网络的形成。