Regulatory Effect of Isomaltodextrin on a High-Fat Diet Mouse Model with LPS-Induced Low-Grade Chronic Inflammation.

This study aimed to identify the effects of isomaltodextrin (IMD) on sustaining the gut integrity and microbiota composition in a high-fat diet (HFD) with a lipopolysaccharide (LPS)-induced low-grade inflammation mouse model. The homeostasis of the immune response is important to reduce the risk of developing metabolic syndromes. The results of this study showed that pre-treatment of IMD at 5% (w/v) suppressed the concentration of endotoxin and pro-inflammatory mediators TNF-α, MCP-1, and IL-6 while increasing the adiponectin level in the plasma. Subsequently, IMD supplementation maintained the structural integrity and intestinal permeability by upregulating the tight junction protein expressions, leading to reducing D-mannitol concentration in the blood. In addition, dysbiosis was observed in mice induced by HFD plus LPS, suggesting that unhealthy dietary factors elicit metabolic endotoxemia and associated dysbiosis to impair the barrier function. However, IMD supplementation was shown to restore the microbial diversity, promote the growth of Bacteroides-Prevotella, and upregulate the related d-glucarate and d-galactarate degradation pathways, together demonstrating the benefits of IMD as a prebiotic able to promote energy homeostasis. Our results also showed that the blood lipid profile and glucose level in the low-grade inflammation mouse model were modulated by IMD. Moreover, IMD supplementation effectively prevented the metabolic disorder and modulated immune responses in inflamed white adipose tissues by inhibiting the macrophage infiltration and restoring the adiponectin, PPAR-γ, and IRS-1 expression. These findings provide strong evidence for IMD to be a potential prebiotic that acts to sustain a healthy gut microbiota composition and barrier function. By protecting against an unhealthy diet-impaired metabolic balance and maintaining immune homeostasis, IMD may affect the development of metabolic disorders.

Development of a method for preparing cyclic nigerosylnigerose syrup and investigation of its value as a dietary fiber.

Cyclic nigerosylnigerose (CNN) syrup, containing 76% water-soluble dietary fiber, was prepared from starch on an industrial scale, using isoamylase, 6-α-glucosyltransferase, 3-α-isomaltosyltransferase, and cyclodextrin glucanotransferase. CNN syrup has a unique linkage pattern, consisting mainly of α-1,3 and α-1,6 glucoside linkages, and is characterized by its low weight average molecular weight (807) and moderate sweetness (relative sweetness = 25), unlike in well-known dietary fiber materials. The glass transition temperature of CNN is higher than that of the straight chain structures, maltotetraose and maltosyltrehalose. Even when 40% of normally added sucrose was replaced with CNN syrup, sponge cake puffed up sufficiently. The no observed adverse effect level for a single dose of CNN syrup was 0.88 and 0.89 g dry solid/kg body weight for men and women, respectively. The increase in blood glucose and insulin concentrations during consumption of CNN syrup was lower than that of glucose.

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.