Egg Yolk Protein Delays Recovery while Ovalbumin Is Useful in Recovery from Iron Deficiency Anemia

Abstract

Protein is a main nutrient involved in overall iron metabolism in vivo. In order to assess the prevention of iron deficiency anemia (IDA) by diet, it is necessary to confirm the influence of dietary protein, which coexists with iron, on iron bioavailability. We investigated the usefulness of the egg structural protein in recovery from IDA. Thirty-one female Sprague-Dawley rats were divided into a control group (n = 6) fed a casein diet (4.0 mg Fe/100 g) for 42 days and an IDA model group (n = 25) created by feeding a low-iron casein diet (LI, 0.4 mg Fe/100 g) for 21 days and these IDA rats were fed normal iron diet with different proteins from eggs for another 21 days. The IDA rats were further divided into four subgroups depending on the proteins fed during the last 21 days, which were those with an egg white diet (LI-W, 4.0 mg Fe/100 g, n = 6), those with an ovalbumin diet (LI-A, 4.0 mg Fe/100 g, n = 7), those with an egg yolk-supplemented diet (LI-Y, 4.0 mg Fe/100 g, n = 6), and the rest with a casein diet (LI-C, 4.0 mg Fe/100 g, n = 6). In the LI-Y group, recovery of the hematocrit, hemoglobin, transferrin saturation level and the hepatic iron content were delayed compared to the other groups (p < 0.01, 0.01, 0.01, and 0.05, respectively), resulting in no recovery from IDA at the end of the experimental period. There were no significant differences in blood parameters in the LI-W and LI-A groups compared to the control group. The hepatic iron content of the LI-W and LI-A groups was higher than that of the LI-C group (p < 0.05). We found that egg white protein was useful for recovery from IDA and one of the efficacious components was ovalbumin, while egg yolk protein delayed recovery of IDA. This study demonstrates, therefore, that bioavailability of dietary iron varies depending on the source of dietary protein.

Keywords: dietary protein; egg-yolk protein; iron deficiency anemia; ovalbumin.

Figure 1

Total iron binding capacity (A); serum iron (B); transferrin saturation (C) on day 21, 26, 31, 36 and 42 after start of experimental period. Iron deficiency anemia rats, fed low iron diet for 21 days, divided four subgroups, was fed either an egg white diet (LI-W, n = 6), an ovalbumin diet (LI-A, n = 7), an egg york diet (LI-Y, n = 6) or a control diet (LI-C, n = 6) and normal rats fed the control diet (C, n = 6) for 42 days. Values were represented as mean. Values with an unlike letter were significant: p < 0.05.

Figure 2

Iron content (A) and hepcidin mRNA expression (B) in the liver, and iron transporter DMT1 (C) and Ferroportin (D) mRNA expression in small intestines on day 42 after start of study. Iron deficiency anemia rats, fed low iron diet for 21 days, divided four subgroups, was fed either an egg white diet (LI-W, n = 6), an ovalbumin diet (LI-A, n = 7), an egg york diet (LI-Y, n = 6) or a control diet (LI-C, n = 6) and normal rats fed the control diet (C, n = 6) for 42 days. The cycle thresholds of the genes of interest were compared with the housekeeping gene β-actin to determine relative changes in expression. Values were represented as means ± SEM. Values with unlike letter were significant: p < 0.05.

Figure 2

Iron content (A) and hepcidin mRNA expression (B) in the liver, and iron transporter DMT1 (C) and Ferroportin (D) mRNA expression in small intestines on day 42 after start of study. Iron deficiency anemia rats, fed low iron diet for 21 days, divided four subgroups, was fed either an egg white diet (LI-W, n = 6), an ovalbumin diet (LI-A, n = 7), an egg york diet (LI-Y, n = 6) or a control diet (LI-C, n = 6) and normal rats fed the control diet (C, n = 6) for 42 days. The cycle thresholds of the genes of interest were compared with the housekeeping gene β-actin to determine relative changes in expression. Values were represented as means ± SEM. Values with unlike letter were significant: p < 0.05.