Abstract
Sucrosomial® Iron is a recently developed formulation to treat iron deficiency based on ferric pyrophosphate covered by a matrix of phospholipids plus sucrose esters of fatty acids. Previous data indicated that Sucrosomial® Iron is efficiently absorbed by iron-deficient subjects, even at low dosage, and without side effects. Its structural properties may suggest that it is absorbed by an intestinal pathway which is different to the one used by ionic iron. Although, studies in vitro showed that Sucrosomial® Iron is readily absorbed, no animal models have been established to study this important aspect. To this aim, we induced iron deficient anemia in mice by feeding them with a low-iron diet, and then we treated them with either Sucrosomial® Iron or sulfate iron by gavage for up to two weeks. Both iron formulations corrected anemia and restored iron stores in a two-week period, but with different kinetics. Ferrous Sulfate was more efficient during the first week and Sucrosomial® Iron in the second week. Of note, when given at the same concentrations, Ferrous Sulfate induced the expression of hepcidin and four different inflammatory markers (Socs3, Saa1, IL6 and CRP), while Sucrosomial® Iron did not. We conclude that anemic mice are interesting models to study the absorption of oral iron, and that Sucrosomial® Iron is to be preferred over Ferrous Sulfate because of similar absorption but without inducing an inflammatory response.
Highlights
Iron deficiency is one of the most common nutritional disorders in the world, and leads to mild or severe anemia and serious consequences in different organs with dramatic effects on life [1]
Ferric iron has to be reduced to Fe(II) by the ferric reductase Duodenal Cytochrome b (Dcytb) of duodenal enterocytes, it passes into the cell cytoplasm via the Divalent Metal Transporter 1 (DMT1) and it is eventually made available to the circulating transferrin after exit via the iron exporter ferroportin expressed at the basolateral side, and re-oxidation to ferric iron by hephaestin [8]
Analysis by were qPCR were performed on samples derived from liver of healthy untreated mice on an iron balanced diet (IB) and mice on iron deficient diet (ID) treated with Saline, Vehicle, Sucrosomial® Iron and Ferrous Sulfate
Summary
Iron deficiency is one of the most common nutritional disorders in the world, and leads to mild or severe anemia and serious consequences in different organs with dramatic effects on life [1]. Frontline treatment of iron deficiency anemia generally consists of oral formulations based on ferrous iron, which is readily absorbed, but that often cause gastrointestinal side effects, such as gastric irritation, nausea, and constipation, that reduce compliance and treatment efficacy [2,3]. SI represents promising tool to treat absolute or functional iron deficiency, but its absorption mechanism remains to be clarified To this end, we comparatively assessed the efficacy of SI and Ferrous Sulfate (FS), administered via gavage, on improving hemoglobin (Hb) levels and iron status, as well as on hepcidin and inflammatory marker response, in a model of iron deficiency anemia in mice. Animal models are important, though, surprisingly, mouse models for the study of iron supplement absorption have not been described so far
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