Marginally excessive iron loading transiently blocks mucosal iron uptake in iron-deficient rats.
Regular "mucosal block" is characterized by decreased uptake of a normal iron load 3-72 h after the administration of excess iron (generally 10 mg) to iron-deficient animals. We found that short-acting mucosal block could be induced by much lower iron concentration and much shorter induction time than previously reported, without affecting levels of gene expression. A rapid endocytic mechanism was reported to decrease intestinal iron absorption after a high iron load, but the activating iron load and the time to decreased absorption were undetermined. We assessed the effects of 30-2,000 μg iron load on iron uptake in the duodenal loop of iron-deficient and iron-sufficient rats under anesthesia. One hour later, mucosal cellular iron uptake in iron-deficient rats administered 30 μg iron was 76.1%, decreasing 25% to 50.7% in rats administered 2,000 μg iron. In contrast, iron uptake by iron-sufficient rats was 63% (range 60.3-65.5%) regardless of iron load. Duodenal mucosal iron concentration was significantly lower in iron-deficient than in iron-sufficient rats. Iron levels in portal blood were consistently higher in iron-deficient rats regardless of iron load, in contrast to the decreased iron uptake on the luminal side. Iron loading blocked mucosal uptake of marginally excess iron (1,000 μg), with a greater effect at 15 min than at 30 min. The rapid induction of short-acting mucosal block only in iron-deficient rats suggests DMT1 internalization.
Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, Hachioji, Tokyo, Japan; and sshinoda@tmu.ac.jp.
Shoko
S
Shinoda
Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, Hachioji, Tokyo, Japan; and.
Shiho
S
Yoshizawa
Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, Hachioji, Tokyo, Japan; and.
Eriko
E
Nozaki
Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, Hachioji, Tokyo, Japan; and.
Kouki
K
Tadai
Department of Food and Nutrition, Jumonji University Niiza, Saitama, Japan.
Anna
A
Arita
D000818:Animals; D001692:Biological Transport; D027682:Cation Transport Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D004386:Duodenum / Q000378:metabolism*; D004705:Endocytosis; D005293:Ferritins / Q000097:blood; D005296:Ferrous Compounds / Q000008:administration & dosage / Q000378:metabolism; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism*; D007501:Iron / Q000008:administration & dosage / Q000097:blood; D000090463:Iron Deficiencies; D019189:Iron Metabolism Disorders / Q000097:blood / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014168:Transferrin / Q000378:metabolism; D000099236:Solute Carrier Family 11, Member 2
D027682:Cation Transport Proteins; D005293:Ferritins; D005296:Ferrous Compounds; D007501:Iron; D014168:Transferrin; D000099236:Solute Carrier Family 11, Member 2; C020748:ferrous sulfate
DMT1; duodenum; excessive iron loading; ferritin; iron absorption; iron deficiency; mucosal block