Abstract
The aim of this study was to investigate the influence of oral iron supplementation, in the form of fortified breads, on the growth performance, health, iron status parameters, and fecal metabolome of anemic piglets. A study was conducted on 24 hybrid (Large White × Landrace × Duroc) piglets. From day 44, the post-natal 12 piglets were supplemented with 100 g of one of two experimental breads, each fortified with 21 mg of ferrous sulphate, either encapsulated or not. After one week of oral supplementation, hematological parameters (hematocrit value, hemoglobin, and red blood cells) showed statistically significant differences (p ≤ 0.05). Piglets fed with the fortified breads had higher iron concentrations in the heart, liver, and intestinal mucosa compared to anemic piglets fed with control bread. Gene expression of hepcidin, iron exporter ferroportin (IREG1), and divalent metal transporter 1 (DMT1), together with concentrations of plasma ferritin, showed no significant statistical differences between groups. Both fortified breads could be used as sources of bioavailable iron. The seven-day intervention trial showed microencapsulation to have only a mild effect on the effectiveness of iron supplementation in the form of fortified bread.
Highlights
Iron is an essential metalloelement for the physiology and biochemistry of most forms of living organism [1]
The presence of ferrous ions in the final experimental breads was determined, as ferrous ions are oxidized to ferric ions, especially under the conditions used in the baking process, which may accelerate the reaction
This study has shown that bread fortified with ferrous sulphate or encapsulated ferrous sulphate provided effective treatment of anemia in piglets
Summary
Iron is an essential metalloelement for the physiology and biochemistry of most forms of living organism [1]. 2 grams of iron is stored by adult men in proteins such as ferritin and hemosiderin, and somewhat less by women of childbearing age. Both the functional and stored iron pools are maintained by the balance between intestinal absorption of dietary iron and iron losses via the gastrointestinal tract, loss of blood (e.g., menstruation), sweat, skin, or urine [4,5]. The absorption of dietary iron is regulated by physiological factors such as bioactive hepcidin peptide, iron importer divalent metal transporter 1 (DMT1), and the cellular iron exporter ferroportin (IREG1) [6]. The molecular target of hepcidin is IREG1, which supplies iron to plasma from duodenal
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