中文摘要：

Dyslipidemia 和长期的发炎在糖尿病的前进起关键作用。这研究试图在糖尿病在多器官在类脂化合物累积上调查煽动性的应力的效果。Eight-week-old 男 db/db 老鼠随机与轮流出现的白天被分到煽动的组有提取的水的每日的注射的 10% 酷蛋白或控制组的下的注射。煽动性的 cytokines 的类脂化合物侧面和血浆层次用临床的生物化学的试金和连接酶的 immunosorbent 试金被决定。在目标机关的类脂化合物累积上的发炎的效果被 hematoxylineosin 染色，染色的油红 O，染色的 Filipin，和量的细胞内部的胆固醇试金评估。低密度的脂蛋白受体(LDLr ) 的蛋白质表情，甾醇规章的元素绑定 protein-2 (SREBP-2 ) ，和在纸巾的 SREBP-cleavage-activating 蛋白质(SCAP ) 被 immunohistochemical 染色并且西方的弄污估计。结果证明煽动性的 cytokines 的浆液层次显著地在注射酷蛋白的老鼠被提高，建议一个煽动的糖尿病的模型被建立。而且，在主动脉，肝，肾，和肠的煽动性的 cytokines 的蛋白质表达式显著地与控制相比在煽动的组被增加。而在煽动的鼠标的类脂化合物一半的浆液层次不与控制相比是不同的，煽动性的应力显著地在主动脉，肝，肾，和肠增加了类脂化合物累积，它在煽动的鼠标的这些机关与 LDLr， SREBP-2，和 SCAP 的增加的蛋白质表达式与一致。在结论，发炎从发行量在 db/db 老鼠的多器官导致类脂化合物累积到外部纸巾，潜在地，由于类脂化合物，再分配由 LDLr 反馈的混乱调停了规定。

英文摘要：

Dyslipidemia and chronic inflammation play crucial roles in the progression of diabetes. This study aimed to investigate the effects of inflammatory stress on lipid accumulation in multi-organs in diabetes. Eight-week-old male db/db mice were randomly assigned to inflamed group with alternating day subcutaneous injection of 10% casein or control group with daily injection of distilled water. The lipid profile and plasma levels of inflammatory cytokines were determined using a clinical biochemical assay and enzyme-linked immunosorbent assay. The effects of inflammation on lipid accumulation in target organs were evaluated by hematoxylin-eosin staining, Oil Red O staining, Filipin staining, and a quantitative intracellular cholesterol assay. The protein expressions of low-density lipoprotein receptor （LDLr）, sterol regulatory element binding protein-2 （SREBP-2）, and SREBP- cleavage-activating protein （SCAP） in tissues were assessed by immunohistochemical staining and western blotting. Results showed that the serum levels of inflammatory cytokines were signifi- cantly elevated in casein-injected mice, suggesting that an inflamed diabetic model was established. Furthermore, the protein expressions of inflammatory cytokines in aortas, livers, kidneys, and intestines were significantly increased in inflamed group compared with control. Whereas the serum levels of lipid moieties in inflamed mice were not different compared with the control, inflammatory stress significantly increased lipid accumulation in aortas, livers, kidneys, and intestines, which coincided with increased protein expressions of LDLr, SREBP-2, and SCAP in these organs of inflamed mice. In conclusion, inflammation induces lipid accumulation in multi-organs of db/db mice from the circulation to peripheral tissues, potentially due to lipid redistribution mediated by the disruption of LDLr feedback regulation.