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In recent years, there have been many reports on the effects of prebiotics on intestinal health. In particular, the consumption of resistant maltodextrin (RMD) has been reported to be beneficial. However, there has been no comprehensive quantification of the effect of RMD on the intestinal environment. Therefore, this study aimed to quantify the effects of RMD on the intestine, especially the intestinal microbiome and metabolome profiles. A randomized, double-blind, and controlled trial was conducted in 29 Japanese subjects, whose hemoglobin A1c (HbA1c) levels are larger than 6% (Clinical trial no. UMIN000023970, https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000027589). The subjects consumed RMD or placebo twice per day for 24 weeks. Blood and fecal samples were collected before and after the intake. The intestinal environment was assessed by a metabologenomics approach, involving 16S rRNA gene-based microbiome analysis and mass spectrometry-based metabolome analysis. The intake of RMD increased the levels of Bifidobacterium and Fusicatenibacter and decreased deoxycholate levels. Additionally, intake of RMD lowered the levels of some opportunistic virulent metabolites, such as imidazole propionate and trimethylamine, in subjects with an initially high amount of those metabolites. RMD may have beneficial effects on the gut environment, such as commensal microbiota modulation and reduction of virulence metabolites, which is known as a causative factor in metabolic disorders. However, the effects of RMD partially depend on the gut environmental baseline.

Enteral nutrition (EN) is a rational approach to providing nutritional intake via the intestines in patients who are unable to tolerate parenteral nutrition. We conducted a preliminary study to investigate the effects of EN on the intestinal environment in 10 patients in a persistent vegetative state (PVS) (n = 5 each in the EN and EN with probiotics; Clostridium butyricum MIYAIRI 588) groups compared with 10 healthy controls. The results of 16S amplicon sequencing of the intestinal microbiota showed that EN led to dysbiosis with a decrease in α-diversity and an obvious change in β-diversity. A particularly significant decrease was seen in useful intestinal bacteria such as Bifidobacterium and butyrate-producing bacteria. Analysis of intestinal metabolites also supported these results, showing significant decreases in butyric and pyruvic acid after EN. Although C. butyricumMIYAIRI 588 improved some intestinal metabolites that were decreased after EN, it did not improve the dysbiosis of the intestinal microbiota. These findings indicate that EN causes dysbiosis of the intestinal microbiota and an imbalance in some intestinal metabolites in patients in a PVS. Moreover, although C. butyricumMIYAIRI 588 improved the imbalance of some intestinal metabolites after EN, it did not prevent dysbiosis of the intestinal microbiota.

Insulin resistance leads to the onset of medical conditions such as type 2 diabetes, and its development is associated with the alteration in the gut microbiota. Although it has been demonstrated that supplementation with prebiotics modulates the gut microbiota, limited evidence is available for effects of prebiotics on insulin resistance, especially for humans. We investigated the prebiotic effect of 1-kestose supplementation on fasting insulin concentration in obesity-prone humans and rats. In the preliminary study using rats, the hyperinsulinemia induced by high-fat diet was suppressed by intake of water with 2% (w/v) 1-kestose. In the clinical study using obese-prone volunteers, the fasting serum insulin level was significantly reduced from 6.5 µU/mL (95% CI, 5.5–7.6) to 5.3 (4.6–6.0) by the 12-week intervention with supplementation of 10 g 1-kestose/day, whereas it was not changed by the intervention with placebo (6.2 µU/mL (5.4–7.1) and 6.5 (5.5–7.6) before and after intervention, respectively). The relative abundance of fecal Bifidobacterium was significantly increased to 0.3244 (SD, 0.1526) in 1-kestose-supplemented participants compared to that in control participants (0.1971 (0.1158)). These results suggest that prebiotic intervention using 1–kestose may potentially ameliorate insulin resistance in overweight humans via the modulation of the gut microbiota. UMIN 000028824.

The relationship between pancreatic ductal adenocarcinoma (PDAC) and the intestinal environment is not fully understood. The purpose of this study was to elucidate the characteristics of the intestinal environment in PDAC. We performed a case-control study of 5 Japanese patients with unresectable PDAC located in the body or tail (PDAC-bt). The number of patients analyzed was limited for this preliminary study. We included 68 healthy subjects, herein control, of pre-printed study in the preliminary study. 16S rRNA amplicon sequencing and metabolomic analysis were performed using fecal samples from the subjects. There was no difference in the Shannon index and Principal Coordinate Analysis between PDAC-bt and the control. However, a significant increase in oral-associated bacteria (Actinomyces, Streptococcus, Veillonella, Lactobacillus) was observed. A significant decrease of Anaerostipes was demonstrated in the feces of PDAC-bt compared with the control. The intestinal propionic acid and deoxycholic acid were significantly lower in PDAC-bt compared with the control. We showed that the intestinal environment of PDAC-bt is characterized by an increase in oral-associated bacteria and an imbalance of metabolites but without changes in alpha and beta diversity of the gut microbiota profiles. Clinical Trial Registration: , UMIN 000041974, 000023675, 000023970. [ABSTRACT FROM AUTHOR]