title: A long-term high-fat diet changes iron distribution in the body, increasing iron accumulation specifically in the mouse spleen.
abstract: 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.
authors.affiliation: Department of Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School.
authors.forename: Noriko
authors.initials: N
authors.lastname: Yamano
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Minoru
authors.initials: M
authors.lastname: Sakama
authors.forename: Yuki
authors.initials: Y
authors.lastname: Izawa-Ishizawa
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Kihira
authors.forename: Keisuke
authors.initials: K
authors.lastname: Ishizawa
authors.forename: Licht
authors.initials: L
authors.lastname: Miyamoto
authors.forename: Shuhei
authors.initials: S
authors.lastname: Tomita
authors.forename: Koichiro
authors.initials: K
authors.lastname: Tsuchiya
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Tamaki
mesh_terms: D000818:Animals; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism*; D059305:Diet, High-Fat / Q000009:adverse effects*; D004041:Dietary Fats / Q000008:administration & dosage* / Q000009:adverse effects; D004386:Duodenum / Q000378:metabolism; D005293:Ferritins / Q000097:blood; D006454:Hemoglobins / Q000378:metabolism; D007408:Intestinal Absorption / Q000235:genetics; D007501:Iron / Q000378:metabolism*; D019266:Iron, Dietary / Q000378:metabolism*; D008297:Male; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000378:metabolism; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D013154:Spleen / Q000378:metabolism*; D000099236:Solute Carrier Family 11, Member 2
chemical_list: D027682:Cation Transport Proteins; D004041:Dietary Fats; D005293:Ferritins; D006454:Hemoglobins; D007501:Iron; D019266:Iron, Dietary; D012333:RNA, Messenger; D000099236:Solute Carrier Family 11, Member 2