Erratum: Attenuation of postprandial blood glucose in humans consuming isomaltodextrin: carbohydrate loading studies.

[This corrects the article DOI: 10.1080/16546628.2017.1325306.].

Inhibitory effect of isomaltodextrin on tyrosine metabolite production in rat gut microbiota.

We examined the effect of isomaltodextrin (IMD), a soluble dietary fiber, on production of putrefactive products by intestinal bacteria using a tyrosine load test to measure phenol production in IMD-treated rats. We observed a significant increase in phenol and p-cresol concentrations in rats administered with only tyrosine, but not for rats co-administered tyrosine and IMD. To elucidate the mechanism of this effect, we analyzed the intestinal microbiota in each group and found that although IMD had no direct effect on the proportion of bacteria known to produce phenols, it did alter the balance of intestinal microbiota. The results suggested that changes in the intestinal microbiota composition reduced the metabolic capacity for tyrosine and in turn suppressed production of phenol or p-cresol, putrefactive products in the intestine.

Anti-Inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-Induced Low-Grade Chronic Inflammation.

：The purpose of this study was to identify the anti-inflammatory activity and mechanism of isomaltodextrin (IMD) in a C57BL/6NCrl mouse model with lipopolysaccharide (LPS)-induced systemic low-grade chronic inflammation and the effect on inflammation-induced potential risk of metabolic disorders. Pre-treatment of IMD decreased the production of pro-inflammatory mediators, TNF-α and MCP-1, and stimulated the production of the anti-inflammatory mediator, adiponectin by increasing the protein expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) in the white adipose tissues. IMD administration reduced plasma concentrations of endotoxin, decreased macrophage infiltration into adipocytes, and increased expression of mucin 2, mucin 4, and the tight junction protein claudin 4. These results suggest that IMD administration exerted an anti-inflammatory effect on mice with LPS-induced inflammation, potentially by decreasing circulating endotoxin, suppressing pro-inflammatory mediators and macrophage infiltration, or by improving mucus or tight junction integrity. IMD exerted protein expression of insulin receptor subset-1 (IRS-1). IMD alleviated the disturbance of gut microflora in LPS-treated mice, as the number of B. bifidum, L. casei, and B. fragilis increased, and E. coli and C. difficile decreased, when compared to LPS-treated mice. The analysis of short chain fatty acids (SCFAs) further supported that the concentrations of acetic and butyric acids were positively correlated with IMD, as well as the number of beneficial bacteria. This study provides evidence that IMD possesses anti-inflammatory properties and exerts beneficial functions to prevent systemic low-grade chronic inflammation and reduces the risk of developing insulin resistance and associated metabolic diseases.

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 T-regs. This study revealed that IMD could be a useful prophylactic candidate for alteration of allergic IR bias in mice and an immune-stimulator for reducing egg induced allergic reactions.

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

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.

Attenuation of postprandial blood glucose in humans consuming isomaltodextrin: carbohydrate loading studies.

Background: Isomaltodextrin (IMD) is a novel highly branched α-glucan and its function as a soluble dietary fiber is expected. Objective: The goal of this study was to evaluate the effects of IMD on postprandial glucose excursions in healthy people and to make the mechanism clear. Design: Twenty-nine subjects ingested a solution containing maltodextrin (MD) or sucrose with or without IMD. Fourteen subjects ingested a solution containing glucose with or without IMD. Blood glucose concentrations were then compared between the groups. Furthermore, in vitro digestion, inhibition of digestive enzymes, and glucose absorption tests were conducted. Results: IMD attenuated blood glucose elevation in the subjects with blood glucose excursions at the high end of normal following the ingestion of MD or sucrose or glucose alone. This effect of 5 g IMD was most clear. IMD was digested partially only by small intestinal mucosal enzymes, and maltase and isomaltase activities were weakly inhibited. Furthermore, IMD inhibited the transport of glucose from mucosal side to serosal side. Conclusions: IMD attenuated postprandial blood glucose, after the ingestion of MD or sucrose or glucose. As one of the mechanism, it was suggested that IMD inhibited the absorption of glucose on small intestinal mucosal membrane.