Atherosclerosis and Nutritional Biochemistry Laboratory, Biochemistry and Immunology Department - Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Anim Sci J. 2012 Jul;83(7):549-55. doi: 10.1111/j.1740-0929.2011.00982.x. Epub 2011 Dec 8.
Apolipoprotein E deficient (Apo E-/-) mice are more resistant to the development of obesity compared to C57BL/6 wild type mice. They also hold a high basal oxidative status due to the loss of antioxidant action of apolipoprotein E. Since obesity is also an inducer of inflammation, we studied the effect of high-fat diet on obesity and oxidative stress in C57BL/6 and Apo E-/- mice for 9 weeks. The results confirmed that Apo E-/- mice fed high-fat diet are more resistant to the increase of both body weight and adiposity compared to C57BL/6 mice. Despite this, Apo E-/- mice presented a higher basal oxidative stress that was enhanced by high-fat diet. Macrophage infiltration, macrophage forming crown-like structures and proinflammatory adipokines (interleukin 6 and tumor necrosis factor alpha) were all higher in adipose tissue from Apo E-/- compared to C57BL/6 mice, regardless of diet type. In conclusion, although Apo E-/- mice are more resistant to becoming obese, they develop more severe adipose tissue inflammation companied by its consequences.
载脂蛋白 E 缺陷（Apo E-/-）小鼠比 C57BL/6 野生型小鼠更能抵抗肥胖的发展。由于载脂蛋白 E 的抗氧化作用丧失，它们还具有较高的基础氧化状态。由于肥胖也是炎症的诱因，我们研究了高脂肪饮食对 C57BL/6 和 Apo E-/-小鼠肥胖和氧化应激的影响，为期 9 周。结果证实，与 C57BL/6 小鼠相比，喂食高脂肪饮食的 Apo E-/-小鼠对体重和体脂增加的抵抗力更强。尽管如此，Apo E-/-小鼠表现出更高的基础氧化应激，高脂肪饮食进一步增强了这种应激。脂肪组织中巨噬细胞浸润、形成冠状结构的巨噬细胞和促炎脂肪因子（白细胞介素 6 和肿瘤坏死因子-α）在 Apo E-/-小鼠中均高于 C57BL/6 小鼠，无论饮食类型如何。总之，尽管 Apo E-/-小鼠更能抵抗肥胖，但它们会发展出更严重的脂肪组织炎症及其后果。
