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Tumour growth in mice resistant to diet-induced obesity

机译:抗小鼠的肿瘤生长抗性饮食诱导的肥胖症

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Obesity is a chronic disease with associated increases in the incidence, and a reduction in survival, of many cancer types. Obesity results from an imbalance in calorie intake and calorie requirement. This study aimed to investigate the separate effects of high-fat diet and obesity on cancer in an animal model resistant to diet-induced obesity. Male BALB/c mice fed long-term on a high-fat, Western-style diet were implanted with syngeneic CT26 colon adenocarcinoma cells and compared to mice fed normal diet. BALB/c mice on high-fat diet were 10% heavier than mice fed normal diet, with no difference in tumour growth rates or tumour cell proliferation. Subgroups of mice that became obese on high-fat diet, however, showed increased tumour growth rates compared to mice fed normal diet, whereas mice that remained slim showed no difference in tumour growth. Protein arrays identified several adipokines that were expressed at different levels, including serum Tissue Inhibitors of Metallo-Proteinases (TIMP-1) and tumour C-Reactive Protein (CRP). In conclusion, tumour growth was enhanced in mice unable to resist obesity, and adipokine profiles were affected by the animals’ ability to resist obesity.
机译:肥胖是一种慢性疾病,发病率相关,以及许多癌症类型的生存率降低。来自卡路里摄入量和卡路里要求的不平衡,肥胖是结果。本研究旨在探讨高脂饮食和肥胖对耐食肥胖症的动物模型中癌症的单独影响。患有高脂肪,西式饮食的雄性Balb / c小鼠植入同工CT26结肠腺癌细胞,与喂养正常饮食的小鼠相比。 Balb / C小鼠在高脂饮食上比喂养正常饮食的小鼠的10%,肿瘤生长速率或肿瘤细胞增殖没有差异。然而,与喂养正常饮食的小鼠相比,对高脂饮食的肥胖的小鼠亚组表现出增加的肿瘤生长率,而仍然薄片的小鼠在肿瘤生长中显示出没有差异。蛋白质阵列鉴定了几种在不同水平表达的脂肪因子,包括金属蛋白酶(TIMP-1)和肿瘤C反应蛋白(CRP)的血清组织抑制剂。总之,在无法抵抗肥胖的小鼠中,肿瘤生长增强,并且己嗪型材受到动物抵抗肥胖症的能力的影响。

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