Yamano Noriko, Ikeda Yasumasa, Sakama Minoru, Izawa-Ishizawa Yuki, Kihira Yoshitaka, Ishizawa Keisuke, Miyamoto Licht, Tomita Shuhei, Tsuchiya Koichiro, Tamaki Toshiaki
Department of Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School.
J Nutr Sci Vitaminol (Tokyo). 2015;61(1):20-7. doi: 10.3177/jnsv.61.20.
Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD.
尽管铁是一种必需的微量金属，但其过量存在会在人体内引发氧化应激。最近的研究表明，铁储存是2型糖尿病的一个风险因素。在小鼠模型中，饮食中铁限制或铁螯合可改善2型糖尿病症状。然而，体内铁含量是否会随着糖尿病的发展而变化尚不清楚。在此，我们研究了通过食用高脂肪饮食而发生肥胖和糖尿病的小鼠（高脂饮食喂养小鼠）中铁积累的动态变化以及铁吸收相关基因的变化。将高脂饮食喂养小鼠（18 - 20周龄）与对照小鼠在血液学特征、血清铁蛋白水平以及腓肠肌、心脏、附睾脂肪、睾丸、肝脏、十二指肠和脾脏中的铁含量方面进行比较。此外，对脾脏进行了组织学检查。还检测了肝脏和十二指肠中铁吸收相关基因的表达。高脂饮食喂养小鼠的血红蛋白和血清铁蛋白水平升高。高脂饮食喂养小鼠在脾脏中出现铁积累，但在心脏或肝脏中未出现。在高脂饮食喂养小鼠中观察到脾红髓和巨噬细胞的百分比增加，并且脾脏中的铁积累主要存在于脾红髓中。高脂饮食喂养小鼠的十二指肠中铁含量也降低。铁吸收相关基因二价金属转运体1（DMT - 1）在高脂饮食喂养小鼠十二指肠中的mRNA表达升高。这些结果表明，由高脂饮食诱导的2型糖尿病的发展会增强铁积累（特别是在脾脏中的积累）。
