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目的探讨高脂饮食诱导的肥胖引起铁缺乏的原因。方法利用高脂饮食16w建立C57BL/6J小鼠肥胖模型,火焰原子吸收法检测肝脏铁水平,RT-PCR检测铁调素(hepcidin)与炎症因子的基因表达,Western blotting检测肝、脾、十二指肠铁代谢相关蛋白的表达。结果与低脂饮食相比,高脂饮食的小鼠存在更高的体质量和更低水平的总铁、游离铁和铁蛋白(ferritin),而肝脏炎症因子白介素-6(IL-6)、白介素1β(IL-1β)、单核细胞趋化因子(MCP-1)及铁调素(hepcidin)表达增加,肝、脾、十二指肠的膜铁输出蛋白(ferroportin)表达下降。同时,高脂饮食的小鼠十二指肠细胞色素b(Dcytb)与二价金属离子转运蛋白1(DMT1)低表达,肝脏DMT1高表达。结论高脂模型下,炎症对肝hepcidin诱导及肠Dcytb下调,可能共同影响十二指肠铁的吸收而导致肥胖小鼠铁缺乏。
Objective To investigate the causes of iron deficiency induced by high-fat diet. Methods C57BL / 6J mice model of obesity was established by high-fat diet for 16 weeks. Iron levels in liver were detected by flame atomic absorption spectrometry. Gene expression of hepcidin and inflammatory cytokines were detected by RT-PCR. Intestinal iron metabolism related protein expression. Results Compared to the low-fat diet, the mice on the high-fat diet had higher body mass and lower levels of total iron, free iron and ferritin, whereas the liver inflammatory factors interleukin-6 (IL-6) The expression of IL-1β, MCP-1 and hepcidin increased, while the expression of ferroportin in liver, spleen and duodenum decreased. At the same time, mice with high-fat diet showed low expression of Dcytb and divalent metal ion transporter 1 (DMT1), and high expression of DMT1 in liver. Conclusion Under the model of hyperlipidemia, inflammation induced hepatic hepcidin and down-regulation of intestinal Dcytb may affect iron absorption in duodenum and lead to iron deficiency in obese mice.