Goat milk consumption modulates liver divalent metal transporter 1 (DMT1) expression and serum hepcidin during Fe repletion in Fe-deficiency anemia.
Iron deficiency is the most prevalent micronutrient deficiency worldwide. In spite of the crucial role of hepatocyte divalent metal transporter 1 (DMT1) and hepcidin in Fe metabolism, to date, no studies have directly tested the role of these proteins in liver Fe metabolism during Fe repletion after induced Fe-deficiency anemia. Therefore, the aim of the current study was to assess the effect of goat or cow milk-based diets on Fe metabolism in one of the main body storage organs, the liver, during the course of Fe repletion with goat or cow milk-based diets in anemic rats. Animals were placed on a preexperimental period of 40 d, a control group receiving a normal-Fe diet and the Fe-deficient group receiving a low-Fe diet (5 mg of Fe/kg of diet). Rats were fed for 30 d with goat or cow milk-based diets with normal Fe content (45 mg of Fe/kg of diet). The hematological parameters, serum hepcidin, hepatosomatic index, liver Fe content, and liver DMT1 expression were determined. During the recovery of the anemia with milk-based diets, the restoration of liver Fe content and hematological parameters, especially with goat milk, increased the red blood cell count, favoring the oxygen supply and weight gain. Moreover, goat milk consumption potentiates liver DMT1 expression, enhancing Fe metabolism and storage. In addition, the increase in serum hepcidin in anemic rats observed in the current study also explains and supports the higher liver Fe content after supplying goat milk, because it blocks the liberation of Fe from hepatocytes, increasing its storage in liver.
Department of Physiology, and.
J
J
Díaz-Castro
Department of Biochemistry and Molecular Biology II, Faculty of Pharmacy, University of Granada and Institute of Nutrition and Food Technology, E-18071 Granada, Spain.
M
M
Pulido
Department of Physiology, and.
M J M
MJ
Alférez
Department of Physiology, and.
J J
JJ
Ochoa
Department of Physiology, and.
E
E
Rivas
Department of Physiology, and.
S
S
Hijano
Department of Physiology, and. Electronic address: milopez@ugr.es.
I
I
López-Aliaga
D018798:Anemia, Iron-Deficiency / Q000097:blood* / Q000178:diet therapy; D000818:Animals; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism*; D002417:Cattle; D004032:Diet / Q000662:veterinary; D004195:Disease Models, Animal; D005293:Ferritins / Q000097:blood; D005786:Gene Expression Regulation; D006041:Goats; D064451:Hepcidins / Q000097:blood*; D007501:Iron / Q000097:blood*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008892:Milk / Q000737:chemistry*; D051381:Rats; D017208:Rats, Wistar; D014168:Transferrin / Q000378:metabolism; D000099236:Solute Carrier Family 11, Member 2
D027682:Cation Transport Proteins; D005293:Ferritins; D064451:Hepcidins; D007501:Iron; D014168:Transferrin; D000099236:Solute Carrier Family 11, Member 2
Fe-deficiency anemia; divalent metal transporter 1; goat and cow milk; serum hepcidin