高脂饮食诱导肥胖引起铁缺乏的机制

发布时间：2018-11-19 21:43

【摘要】：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。
[Abstract]:Objective to investigate the causes of iron deficiency induced by high fat diet. Methods the obesity model of C57BL/6J mice was established by high fat diet for 16 weeks. The iron levels in liver were detected by flame atomic absorption spectrometry, and the expression of iron modulin (hepcidin) and inflammatory factor gene by, Western blotting were detected by RT-PCR. The liver and spleen were detected by, Western blotting. Expression of iron metabolism-related proteins in duodenum. Results compared with low-fat diet, mice with high fat diet had higher body weight and lower total iron, free iron and ferritin (ferritin), and liver inflammatory factors such as interleukin-6 (IL-6) and interleukin-1 尾 (IL-1 尾). The expression of monocyte chemokine (MCP-1) and iron modulin (hepcidin) increased, while the expression of membrane iron exportation protein (ferroportin) in liver, spleen and duodenum decreased. At the same time, the expression of cytochrome b (Dcytb) and divalent metal ion transporter 1 (DMT1) in the duodenum of mice with high fat diet was low, and the expression of DMT1 in liver was high. Conclusion in hyperlipidemia model, inflammation induced by liver hepcidin and down-regulation of intestinal Dcytb may jointly affect iron absorption in duodenum and lead to iron deficiency in obese mice.
【作者单位】：华中科技大学同济医学院公共卫生学院营养与食品卫生学系;
【基金】：国家自然科学基金(No.0204513184)
【分类号】：R151

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