Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.
Vet Pathol. 2010 Mar;47(2):202-13. doi: 10.1177/0300985809357753. Epub 2010 Feb 1.
In recent years, obesity has been identified as a risk factor for the development of breast cancer in postmenopausal women, and it has been associated with a poor outcome. Many factors appear to be important in the mechanism of this increased risk, including estrogen, estrogen receptors, and the adipokines leptin and adiponectin. Estrogen, a potent mitogen for mammary cells, has long been implicated in the development of mammary tumors. Because adipose-associated aromatase activity increases the conversion of androgen to estrogen, mammary adipose tissue is thought to be an important source of local estrogen production. Leptin, which increases in the circulation in proportion to body fat stores, has been demonstrated in vitro to promote breast cancer cell growth. Animal models have also identified leptin as an important factor for the development of mammary tumors. In contrast to leptin, serum adiponectin concentrations are inversely related to body fat stores, and the addition of adiponectin to human breast cancer cells reduces cell proliferation and enhances apoptosis. This review explores the relationship between these factors and the development of mammary cancer in humans and mouse models.
近年来，肥胖已被确定为绝经后妇女乳腺癌发展的一个风险因素，并且与不良预后相关。许多因素似乎在这种风险增加的机制中很重要，包括雌激素、雌激素受体以及脂肪因子瘦素和脂联素。雌激素是乳腺细胞的一种强有力的有丝分裂原，长期以来一直被认为与乳腺肿瘤的发展有关。因为脂肪相关的芳香酶活性增加了雄激素向雌激素的转化，所以乳腺脂肪组织被认为是局部雌激素产生的重要来源。瘦素与体脂肪储存成正比地增加循环，已在体外证明可促进乳腺癌细胞生长。动物模型也确定了瘦素是乳腺肿瘤发展的重要因素。与瘦素相反，血清脂联素浓度与体脂肪储存呈反比，并且将脂联素添加到人乳腺癌细胞中可减少细胞增殖并增强细胞凋亡。这篇综述探讨了这些因素与人类和小鼠模型中乳腺癌的发展之间的关系。
