Nunez Nomeli P, Hursting Stephen D, Yakar Shoshana, Fowler Dan, Vinson Charles
Division of Nutritional Sciences, University of Texas, Austin, TX, USA.
Methods Mol Biol. 2009;512:29-37. doi: 10.1007/978-1-60327-530-9_3.
Current dogma suggests that the positive correlation between obesity and cancer is driven by white adipose tissue that accompanies obesity, possibly through excess secretion of adipokines. However, recent studies in fatless A-Zip/F-1 mice, which have undetectable adipokine levels but display accelerated tumor formation, suggest that adipokines are not required for the enhanced tumor development. The A-Zip/F-1 mice are also diabetic and display elevated circulating levels of other molecules frequently associated with obesity and carcinogenesis: insulin, insulin-like growth factor-1, and inflammatory cytokines. Therefore, we postulate that the pathways associated with insulin resistance and inflammation, rather than adipocyte-derived factors, may represent key prevention or therapeutic targets for disrupting the obesity-cancer link.
当前的理论认为，肥胖与癌症之间的正相关关系是由伴随肥胖出现的白色脂肪组织驱动的，可能是通过脂肪因子的过量分泌。然而，最近对无脂肪的A-Zip/F-1小鼠的研究表明，脂肪因子对于增强肿瘤发展并非必需，这些小鼠的脂肪因子水平无法检测到，但肿瘤形成加速。A-Zip/F-1小鼠也是糖尿病模型，其循环中其他经常与肥胖和致癌作用相关的分子水平升高：胰岛素、胰岛素样生长因子-1和炎性细胞因子。因此，我们推测，与胰岛素抵抗和炎症相关的通路，而非脂肪细胞衍生因子，可能是破坏肥胖与癌症联系的关键预防或治疗靶点。
