Prophylactic effects of isomaltodextrin in a Balb/c mouse model of egg allergy

The aim of this study was to evaluate the potential effects of isomaltodextrin (IMD), a dietary saccharide polymer derived from enzymatically produced from starch, on the ability to alter immune response (IR) bias to hen egg ovalbumin (Ova) induced allergic inflammation in mice. Groups of Balb/c mice were pre-treated with various doses of IMD in drinking water (1.0, 2.5, and 5.0% w/v) for 6 weeks and subsequently sensitized to the Ova together with continuous administration of IMD. To evaluate changes in immune response bias, immunoglobulin isotype-associated antibody activity, concentrations of type 1 and 2 cytokines and the percentage of T-regulatory cells (T-regs) in blood were measured. Clinical signs of allergy were assessed after oral challenge with Ova. Treatment with IMD did not significantly alter the frequency of clinical signs, however there was a trend in the overall reduction of clinical signs. Effect on IR bias was observed in the treatment groups as reflected by reduction in a type 1-biased phenotype as evident by decrease in isotype-specific IgE, IgG and increase in IL-12 cytokine production and a high proportion of Tregs. This study revealed that IMD could be a useful prophylactic candidate for alteration of allergic IR bias in mice and an immunestimulator for reducing egg induced allergic reactions

Prophylactic effects of isomaltodextrin in a Balb/c mouse model of egg allergy

The aim of this study was to evaluate the potential effects of isomaltodextrin (IMD), a dietary saccharide polymer derived from enzymatically produced from starch, on the ability to alter immune response (IR) bias to hen egg ovalbumin (Ova) induced allergic inflammation in mice. Groups of Balb/c mice were pre-treated with various doses of IMD in drinking water (1.0, 2.5, and 5.0% w/v) for 6 weeks and subsequently sensitized to the Ova together with continuous administration of IMD. To evaluate changes in immune response bias, immunoglobulin isotype-associated antibody activity, concentrations of type 1 and 2 cytokines and the percentage of T-regulatory cells (T-regs) in blood were measured. Clinical signs of allergy were assessed after oral challenge with Ova. Treatment with IMD did not significantly alter the frequency of clinical signs, however there was a trend in the overall reduction of clinical signs. Effect on IR bias was observed in the treatment groups as reflected by reduction in a type 1-biased phenotype as evident by decrease in isotype-specific IgE, IgG and increase in IL-12 cytokine production and a high proportion of Tregs. This study revealed that IMD could be a useful prophylactic candidate for alteration of allergic IR bias in mice and an immunestimulator for reducing egg induced allergic reactions

Effects of isomaltodextrin in postprandial lipid kinetics: Rat study and human randomized crossover study

<div><p>Isomaltodextrin (IMD) is a novel dietary fiber-like polysaccharide: a type of α-glucan produced from starch using enzymes derived from microorganisms. The results of cohort studies show that dietary fiber can prevent cardiovascular disorders caused by lifestyle-related diseases such as metabolic syndrome. Inhibition of excess fat absorption by dietary fiber is known to be one of the mechanisms, and it is also known that the actions of dietary fiber vary depending on factors such as its structure or origin. Thus, we investigated the inhibitory actions of IMD on fat absorption, and analyzed its mechanism of action. In rats, the absorption of fat given by gavage was significantly lower at 1, 2, and 6 hours after IMD administration than after vehicle administration. In humans, IMD was associated with a lesser increase in blood triglycerides in subjects whose blood triglycerides were otherwise apt to rise. We also found by in vitro emulsion studies that IMD, which had no effect on digestive enzyme activity or emulsion formation, stabilized the micro size micelle by inducing enlarged micelle particle size and increased zeta potential. In conclusion, the mechanism of inhibition of fat absorption by IMD may be a delay in micelle particles accessing the intestinal epithelium through changes in the surface structure and the physical properties of the micelle particles.</p></div

C_max and AUC of triglyceride and blood remnant-like particle cholesterol.

<p>C_max and AUC of triglyceride and blood remnant-like particle cholesterol.</p

Physical properties of micelles.

<p>(A) Changes in particle size after adding IMD. (B) Changes in zeta potential after adding IMD. Control: 150 mM phosphate buffer; particle size (n = 3); zeta potential (n = 5). Low IMD: 0.1 g/mL IMD in 150 mM phosphate buffer; particle size (n = 3); zeta potential (n = 4). High IMD: 0.2 g/mL IMD in 150mM phosphate buffer; particle size (n = 3); zeta potential (n = 5). Values are mean ± standard error. Statistical analyses were performed using Tukey-Kramer multiple comparison tests. Different letters indicate significant differences: p <0.05.</p

Triglyceride kinetics in blood.

<p>(A) Transition blood TG levels in time after lipid loading. (B) Area under the blood concentration-time curve. ○: Control (1.5 g/kg-bw oil); n = 6, △: Low IMD (1.5 g/kg-bw oil + 0.2 g/kg-bw IMD); n = 5, ●: High IMD (1.5 g/kg-bw oil + 1.0 g/kg-bw IMD); n = 6. Values are mean ± standard deviation (n = 5 or 6). Statistical analyses were performed using a Tukey-Kramer multiple comparison test (vs control: *p <0.05, **p <0.01).</p

Trial flow chart.

<p>Trial flow chart.</p

The putative structure of IMD.

<p>The putative structure of IMD.</p