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首页> 外文期刊>Genes and Nutrition >Impaired leptin activity in New Zealand Obese mice: model of angiogenesis
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Impaired leptin activity in New Zealand Obese mice: model of angiogenesis

机译:新西兰肥胖小鼠的瘦素活性受损:血管生成模型

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摘要

Leptin is prompt to drive angiogenesis, effecting proper vascularisation. Tissue remodeling (including adipose organ) is associated with the angiogenic response. The aim of this study was to investigate the effect of hyperleptinemia on angiogenesis in subcutaneous (s.c.) in vivo matrigel model in mice on a high fat (HF) diet. HF promoted adipose tissue accumulation and biochemical changes resembling metabolic syndrome. However, the impact of this dietary treatment on angiogenesis, measured in s.c. matrigel model was not significant. Changes in leptin concentration were not accompanied by significant angiogenic response. This lack of leptin activity and impaired signal transduction at the molecular level suggests malfunction of the leptin receptor in NZO mice.
机译:瘦素提示驱动血管生成,影响适当的血管形成。组织重塑(包括脂肪器官)与血管生成反应有关。这项研究的目的是研究高脂饮食对高脂(HF)饮食小鼠体内皮下(s.c.)体内基质胶模型中血管生成的影响。 HF促进了脂肪组织的积累和类似于代谢综合征的生化变化。但是,这种饮食疗法对血管生成的影响(以秒为单位)。 Matrigel模型不显着。瘦素浓度的变化不伴有明显的血管生成反应。瘦素活性的缺乏和在分子水平上信号传导的减弱暗示了NZO小鼠中瘦素受体的功能异常。

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