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Obesity is regarded as a global concern with increasing prevalence, most notably in developed countries. Metabolic syndrome is a predictor of cardiovascular disease and type 2 diabetes mellitus and is defined as the accumulation of multiple risk factors caused by abdominal visceral obesity. Resistant maltodextrin (RMD) is a soluble dietary fiber that has been shown to reduce visceral fat in long-term clinical trials when continuously administered at 10 g, three times daily. Herein, we evaluated the effects of long-term consumption of 5 g RMD three times daily. A total of 140 healthy adults were randomly assigned to two intervention groups for a 12-wk randomized, double-blind, placebo-controlled, parallel-group trial. Participants ingested a test beverage containing 5 g RMD or a placebo beverage without RMD. Interviews, anthropometric measurements, physiological examination, blood tests, and urinalyses were conducted at baseline and every 4 wk during the trial. Computed tomography scans were performed at baseline and at the end of week 8 and 12. Results showed that abdominal visceral fat area (VFA) significantly decreased in the test group from 105.33±26.83 cm2 at baseline to 101.15±24.33 cm2 at week 12. Further, a significant difference was observed in the VFA between the test and control groups (p

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.

ObjectiveIn recent years, there have been many reports on the effects of prebiotics on intestinal health. In particular, consuming 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.DesignA randomized, double-blind controlled trial was conducted in 29 Japanese subjects with relatively high hemoglobin A1c (HbA1c). Subjects consumed RMD or placebo twice per day for 24 weeks. Blood and fecal samples were collected before and after intake. The intestinal environment was assessed by a metabologenomics approach combined with 16S rRNA gene-based microbiome and mass spectrometry-based metabologenomics analyses.ResultsThe intake of RMD increased the levels of Bifidobacterium and Fusicatenibacter, and decreased deoxycholate. In addition, intake of the RMD lowered the levels of some virulent metabolites, such as imidazole propionate and trimethylamine, in subjects with an initially high amount of those metabolites.ConclusionRMD may have beneficial effects on the gut environment such as commensal microbiota modulation and reduction of virulence metabolites, known as a causative factor in metabolic disorders. However, its effect partially depends on the gut environmental baseline.

Quantitative analysis of glycans released from glycoproteins using high-performance liquid chromatography (HPLC) requires fluorescent tag labeling to enhance sensitivity and selectivity. However, the methods required to remove large amounts of excess labeling reagents from the reaction mixture are time-consuming. Furthermore, these methods, including solvent extraction and solid phase extraction (SPE), often impair quantitative analysis. Here, we developed an online sample cleanup procedure for HPLC analysis of 2-aminopyridine (AP)-labeled glycans using a six-port/two-way valve and two small columns: one packed with a strong cation exchange resin (SCX) and the other comprising ODS silica gel. AP-labeled glycans delivered from an injection port were separated from excess AP by passing through an SCX column (4.6 mm i.d., 1 cm long) regulated to 40°C. The AP-labeled glycans were trapped on an ODS column (4.6 mm i.d., 1 cm long) to further separate them from inorganic contaminants. By changing the valve position after 2 min to connect the ODS column to an analysis column, AP-labeled glycans trapped in the ODS column were eluted with an acetonitrile-containing eluent followed by hydrophilic interaction liquid chromatography (HILIC) separation on an amide column or reversed-phase mode separation on a C30 column. This method was successfully used to analyze N-linked glycans released from several glycoprotein samples.

Glucagon-like peptide 1 (GLP-1), an incretin gastrointestinal hormone, is secreted when stimulated by nutrients including metabolizable sugars such as glucose and fructose. d -Allulose (allulose), also known as d -psicose, is a C-3 isomer of d -fructose and a rare sugar with anti-diabetic or anti-obese effects in animal models. In the present study, we examined whether an oral administration of allulose could stimulate GLP-1 secretion in rats, and investigated the underlying mechanisms. Oral, but not intraperitoneal, administration of allulose (0.5–2.0 g/kg body weight) elevated plasma GLP-1 levels for more than 2 h in a dose-dependent manner. The effects of allulose on GLP-1 secretion were higher than that of dextrin, fructose, or glucose. In addition, oral allulose increased total and active GLP-1, but not glucose-dependent insulinotropic polypeptide (GIP), levels in the portal vein. In anesthetized rats equipped with a portal catheter, luminal (duodenum and ileum) administration of allulose increased portal GLP-1 levels, indicating the luminal effect of allulose. Allulose-induced GLP-1 secretion was abolished in the presence of xanthohumol (a glucose/fructose transport inhibitor), but not in the presence of inhibitors of the sodium-dependent glucose cotransporter 1 or the sweet taste receptor. These results demonstrate a potent and lasting effect of orally administered allulose on GLP-1 secretion in rats, without affecting GIP secretion. The potent and selective GLP-1-releasing effect of allulose holds promise for the prevention and treatment of glucose intolerance through promoting endogenous GLP-1 secretion.

Purpose Increasing secretion and production of glucagon-like peptide-1 (GLP-1) by continuous ingestion of certain food components has been expected to prevent glucose intolerance and obesity. In this study, we examined whether a physiological dose (5% weight in diet) of digestion-resistant maltodextrin (RMD) has a GLP-1-promoting effect in rats fed a high-fat and high-sucrose (HFS) diet. Methods Rats were fed a control diet or the HFS (30% fat, 40% sucrose wt/wt) diet supplemented with 5% RMD or fructooligosaccharides (FOS) for 8 weeks or for 8 days in separated experiments. Glucose tolerance, energy intake, plasma and tissue GLP-1 concentrations, and cecal short-chain fatty acids concentrations were assessed. Results After 4 weeks of feeding, HFS-fed rats had significantly higher glycemic response to oral glucose than control rats, but rats fed HFS?+?RMD/FOS did not (approx. 50% reduction vs HFS rats). HFS?+?RMD/FOS-fed rats had higher GLP-1 responses (~twofold) to oral glucose, than control rats. After 8 weeks, visceral adipose tissue weight was significantly higher in HFS-fed rats than control rats, while HFS?+?RMD/FOS rats had a trend of reduced gain (~50%) of the tissue weight. GLP-1 contents and luminal propionate concentrations in the large intestine increased (>twofold) by adding RMD/FOS to HFS. Eight days feeding of RMD/FOS-supplemented diets reduced energy intake (~10%) and enhanced cecal GLP-1 production (~twofold), compared to HFS diet. Conclusions The physiological dose of a prebiotic fiber promptly (within 8 days) promotes GLP-1 production in rats fed an obesogenic diet, which would help to prevent excess energy intake and fat accumulation.

In HPLC analyses of soluble dietary fiber, desalting processes using open, mixed-bed ion-exchange columns are time-consuming and labor-intensive. We developed and validated a simple desalting method using tandem cation/anion exchange SPE cartridges. We found that combining Bond Elut Jr SCX (upstream) and Bond Elut PSA (downstream) cartridges provided adequate desalting of test solutions. The developed method was then validated in an inter-laboratory study. Five test samples were prepared by mixing food matrixes with purified soluble dietary fiber and treated to generate solutions to test the desalting process. These solutions were then analyzed by eight different laboratories. The results demonstrated that the developed method is simple and reliable for desalting samples containing 140 to 945 mg/100 mL of soluble dietary fiber in preparation for HPLC analysis of soluble dietary fiber.

Several studies have suggested that resistant maltodextrin (RMD) suppresses intestinal lipid absorption in experimental animals and humans. However, possible mechanisms underlying this effect are not known. In this study, effects of RMD on processes of the absorption of various lipids were investigated in vitro. RMD dose-dependently suppressed the solubility of various lipid components, including 1-mono-oleoylglycerol, oleic acid, and phosphatidylcholine in bile salt micelles in vitro. When the diffusion rate of bile salt micelles through a filter membrane was investigated in vitro, bile salt micelles containing RMD diffused more slowly than those without RMD. Incorporation of [1-14C] oleic acid into Caco-2 cells from the RMD-containing bile salt micelles was significantly smaller than that from the control micelles (without RMD). These results show that RMD suppresses intestinal absorption of lipids by decreasing their micellar solubility and the diffusion rate of bile salt micelles.

Resistant maltodextrin (RMD) is a soluble dietary fibre that exerts several physiological functions as a result of its microbial degradation and changes in the intestinal environment. It has been reported that RMD enhanced immunoglobulin A (IgA) secretion, which protects the mucosa from foreign substances. However, the effect of RMD on excessive immunity has yet to be investigated. In this study, we aimed to investigate the effect of RMD on excessive immune responses such as food allergy. OVA23-3 mice were fed an AIN-76-based diet containing 20% egg-white protein with or without RMD. While RMD was shown to contribute to an increase in goblet cells, RMD did not change the overall inflammatory status when ingested with the egg-white diet. RMD suppressed IL-4 and IL-10 production from splenocytes but not cells from mesenteric lymph nodes. RMD also downregulated the serum levels of OVA-specific Th1- and Th2-related antibodies, which were elevated in the food-allergic condition. RMD significantly increased the total amount of short-chain fatty acids, especially acetate and propionate, in the caecum of OVA23-3 mice fed the egg-white diet. Our study demonstrated that dietary RMD modulates systemic rather than intestinal antigen-specific immune responses in the food-allergic condition of OVA23-3 mice. Although the relevant mechanism has yet to be investigated, RMD shows potential for alleviating food allergy through adjustment of systemic immunity.

Glucagon-like peptide-1 (GLP-1), which is produced and released from enteroendocrine L cells, plays pivotal roles in postprandial glycaemia. The ingestion of resistant maltodextrin (RMD), a water-soluble non-digestible saccharide, improves the glycaemic response. In the present study, we examined whether the continuous feeding of RMD to rats affected GLP-1 levels and glycaemic control. Male Sprague–Dawley rats (6 weeks of age) were fed an American Institute of Nutrition (AIN)-93G-based diet containing either cellulose (5 %) as a control, RMD (2·5 or 5 %), or fructo-oligosaccharides (FOS, 2·5 or 5 %) for 7 weeks. During the test period, an intraperitoneal glucose tolerance test (IPGTT) was performed after 6 weeks. Fasting GLP-1 levels were significantly higher in the 5 % RMD group than in the control group after 6 weeks. The IPGTT results showed that the glycaemic response was lower in the 5 % RMD group than in the control group. Lower caecal pH, higher caecal tissue and content weights were observed in the RMD and FOS groups. Proglucagon mRNA levels were increased in the caecum and colon of both RMD and FOS groups, whereas caecal GLP-1 content was increased in the 5 % RMD group. In addition, a 1 h RMD exposure induced GLP-1 secretion in an enteroendocrine L-cell model, and single oral administration of RMD increased plasma GLP-1 levels in conscious rats. The present study demonstrates that continuous ingestion of RMD increased GLP-1 secretion and production in normal rats, which could be stimulated by its direct and indirect (enhanced gut fermentation) effects on GLP-1-producing cells, and contribute to improving glucose tolerance.

Anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID) is caused by mutations in the NF-κB essential modulator (NEMO) or NF-κB inhibitor, alpha (IKBA) genes. A heterozygous NEMO mutation causes incontinentia pigmenti (IP) in females, while a hemizygous hypomorphic mutation of NEMO causes EDA-ID in males. In general, immunodeficiency is not shown in IP patients. Here, we investigated two female patients with IP and immunodeficiency. The patients were initially suspected to have IRAK4 deficiency and Mendelian susceptibility to mycobacterial disease, respectively, because of recurrent pneumonia with delayed umbilical cord detachment or disseminated mycobacterial infectious disease. We measured tumor necrosis factor (TNF)-α production and performed mutation screening. The TNF-α production from lipopolysaccharide (LPS)-stimulated CD14-positive cells was partially defective in both female patients. A genetic analysis showed them to carry the heterozygous NEMO mutations c.1167_1168insC or c.1192C>T. Although NEMO mutations in IP patients are typically eliminated by X-inactivation skewing, an analysis of cDNA obtained from the somatic cells of the patients showed the persistence of these mutations in peripheral blood mononuclear cells and peripheral granulocytes. A NF-κB reporter gene analysis using NEMO-deficient HEK293 cells showed the loss of NF-κB activity in these NEMO mutants, while the NF-κB protein expression levels by the NEMO mutants were consistent with those of wild-type NEMO. The delayed skewing of the mutant allele may be responsible for the observed innate immune defect in these patients. The detection of LPS unresponsiveness is suitable for identifying female IP patients with immunodeficiency.

A series of safety assessments were performed on hydrogenated resistant maltodextrin prepared by converting the reducing terminal glucose of resistant maltodextrin into sorbitol. The reverse mutation assay did not show mutagenicity. Acute and 90-day subchronic oral toxicity studies in rats showed no death was observed in any groups, including the group receiving the highest single dose of 10 g/kg body weight or the highest dose of 5 g/kg body weight per day for 90 days. Mucous or watery stools were observed in the hydrogenated resistant maltodextrin treatment group on the acute study, which were transient and were associated with the osmotic pressure caused by intake of the high concentrations. Subchronic study showed dose-dependent increases in the weights of cecum alone, cecal contents alone, and cecum with cecal contents as well as hypertrophy of the cecal mucosal epithelium, which are considered to be common physiological responses after intake of indigestible carbohydrates. These results indicated that the no observed adverse effect level (NOAEL) of hydrogenated resistant maltodextrin was 10 g/kg body weight or more on the acute oral toxicity study and 5.0 g/kg body weight/day or more on the 90-day subchronic repeated oral toxicity study in rats. Further study performed in healthy adult humans showed that the acute no-effect level of hydrogenated resistant maltodextrin for diarrhea was 0.8 g/kg body weight for men and more than 1.0 g/kg body weight for women. The results of the current safety assessment studies suggest that hydrogenated resistant maltodextrin is safe for human consumption.

Experiments with rats have produced data on the metabolism and energy value of d-psicose; however, no such data have been obtained in humans. The authors assessed the availability of d-psicose absorbed in the small intestine by measuring carbohydrate energy expenditure (CEE) by indirect calorimetry. They measured the urinary excretion rate by quantifying d-psicose in urine for 48 hours. To examine d-psicose fermentation in the large intestine, the authors measured breath hydrogen gas and fermentability using 35 strains of intestinal bacteria. Six healthy subjects participated in the CEE test, and 14 participated in breath hydrogen gas and urine tests. d-Psicose fermentation subsequent to an 8-week adaptation period was also assessed by measuring hydrogen gas in 8 subjects. d-Psicose absorbed in the small intestine was not metabolized into energy, unlike glucose, because CEE did not increase within 3 hours of d-psicose ingestion (0.35 g/kg body weight [BW]). The accumulated d-psicose urinary excretion rates were around 70% for 0.34, 0.17, and 0.08 g/kg BW of ingested d-psicose. Low d-psicose fermentability was observed in intestinal bacteria and breath hydrogen gas tests, in which fructooligosaccharide (0.34, 0.17, and 0.08 g/kg BW) was used as a positive control because its available energy is known to be 8.4 kJ/g. Based on the results of the plot of breath hydrogen concentration vs calories ingested, the energy value of d-psicose was expected to be less than 1.6 kJ/g. Incremental d-psicose fermentability subsequent to an adaptation period was not observed.

Background: It has been reported that low-viscous and fermentable dietary fiber and nondigestible oligosaccharides enhance mineral absorption. Resistant maltodextrin, nonviscous, fermentable and soluble source of dietary fiber, has several physiological functions. However, influence of resistant maltodextrin on mineral absorption is unclear. Aim of the study: We conducted balance studies in rats to investigate effects of resistant maltodextrin and hydrogenated resistant maltodextrin on apparent mineral absorption. Methods: In experiment 1 (Exp. 1), 40 rats were fed test diets based on AIN-93G with or without resistant maltodextrin or hydrogenated resistant maltodextrin for 2 weeks. In experiment 2 (Exp. 2), 32 rats were cecectomized (CX) or sham-operated (Sham) and fed diets with or without hydrogenated resistant maltodextrin for 1 week. Results: In Exp. 1, ingestion of resistant maltodextrin and hydrogenated resistant maltodextrin dose-dependently enhanced apparent absorption rates of Ca, Mg, Fe and Zn, and increased cecal fermentation with cecal expansion. In Exp. 2, the absorption rates of Ca and Mg were significantly enhanced by ingestion of hydrogenated resistant maltodextrin in Sham group but not in CX group. The promotion of Fe and Zn absorption was not affected by cecectomy. Conclusion: Ingestion of resistant maltodextrin and hydrogenated resistant maltodextrin increased apparent Ca and Mg absorptions dependent on cecal fermentation, while other mechanisms may also be involved in promotion of apparent Fe and Zn absorption by resistant maltodextrin.

In order to confirm the mechanism how postprandial elevation of triacylglycerol is suppressed by resistant maltodextrin (Fibersol-2), we conducted the following experiments. Firstly, Rats were fed a high-fat diet with resistant maltodextrin at 0% (control), 2.5% or 5% for 5 weeks to determine the lipid amount excreted in the feces of the last three days. The total lipid and triacylglycerol excreted in rat feces were significantly increased in a dose-dependent manner by the ingestion of resistant maltodextrin. Secondly, 10 healthy adult subjects were administrated a beverage containing 5 g resistant maltodextrin or placebo for 10 days, and crossed over after an 11-day washout. Total lipid excreted in feces was determined by collecting all the feces for the last three days. Fecal weight and fecal lipid amount of the subjects increased significantly with the ingestion of resistant maltodextrin compared to the placebo ingestion. Thirdly, oil emulsion prepared with resistant maltodextrin was assessed for its hydrolysis rate by lipase. The hydrolysis rate of lipid by lipase was not affected by resistant maltodextrin. Lastly, micelle emulsion was prepared with or without resistant maltodextrin, and their stability was compared. Resistant maltodextrin inhibited the decomposition of micelles and stabilized micellar structure. From these results, it was suggested that resistant maltodextrin suppresses lipid absorption and promotes the excretion of lipid into feces by delaying the release of fatty acids from micelles in the lipid absorption process. No inhibitory effect on lipase activity was observed by resistant maltodextrin.

還元難消化性デキストリンの食後血糖値に及ぼす影響を動物実験およびヒト試験において検討した。SD系雄性ラットを用い, 還元難消化性デキストリンを2.5-80%添加した糖負荷試験の結果, 5%添加で最も強い抑制効果がみられ, それ以上の添加においても同等の効果を示した。また, 健常成人男女9名を対象とし, 還元難消化性デキストリンを2.5-10g添加した食事負荷試験の結果, 5g以上の添加で有意な抑制効果が認められ, 用量依存性が認められた。次に健常成人男女10名を対象として還元難消化性デキストリンおよび難消化性デキストリンをそれぞれ5g添加した際の血糖上昇抑制効果を比較した結果, その効果はほぼ同等であることが確認された。これらの結果から, 還元難消化性デキストリンは食後血糖上昇抑制効果を有し, その効果の程度は難消化性デキストリンと同等であることが確認された。

In 1988 we recognized glycosylated components in pyrodextrin and started a study to obtain an amylase-resistant ingredient. We succeeded in establishing a series of processes for industrial-scale separation of the indigestible component with superior appearance and taste by roasting starch (pyrolysis), enzymatic hydrolysis, purification, chromatographic fractionation and spray drying. The component was named indigestible dextrin (ID). In order to utilize ID as a source of dietary fiber, a low-calorie ingredient, and a physiologically active ingredient, we first confirmed that ID is a highly safe ingredient by conducting an acute toxicity study, a mutagenicity study, long-term administration studies in both rats and humans, and a study of diarrhea caused by long-term consumption. A novel determination method using the enzyme-gravimetric method in combination with high performance liquid chromatography (enzyme-HPLC method) was proposed to the Association of Official Analytical Chemists (AOAC) and approved as Final Action Method AOAC 2001. 03 in January 2005. Animal and human studies showed the energy value of 1 kcal/g dietary fiber fraction. Based on these results, ID has been approved in many countries. Moreover, it has been confirmed by both animal and clinical studies that ID has physiological functions such as intestinal regularity, moderating postprandial blood glucose level, lowering serum lipid, and reducing body fat. As for the physicochemical properties of ID, it is similar to DE 10 maltodextrin in sweetness and browning property. The properties of not being fermented easily by yeast or lactobacillus impart an interesting characteristic to beer and lactic acid drinks. At present ID is commercially available for use in a wide range of food products not only in Japan but also in many countries around the world.

We developed a branched corn syrup (BCS, average molecular weight: 500, content of indigestible portion: 45%) by heat treatment of indigestible dextrin with hydrochloric acid. To confirm the safety of BCS, we conducted both an acute toxicity test and a mutagenicity test. Moreover, we observed gastroenteric effects of BCS in fifty healthy humans. The results are summarized as follows. 1) There was no death observed after oral administration of BCS in Sprague-Dawley-strain rats. Lethal dose (LD)50, value was estimated to be more than 10 g/kg body weight. 2) No mutagenicity was observed in Salmonella typhimurium TA98, TA100, TA1535, TA1537, or Escherichia coli WP2uvrA. 3) Fifty adults were divided into five groups often (five of each sex) and orally administered BCS at 0.2, 0.3, 0.4. 0.5 and 0.6 g/kg body weight as indigestible portion. Although no diarrhea was observed in females, BCS at 0.6 g/kg as indigestible portion caused diarrhea in two out of five males. The maximum non-effective dose of indigestible portion of BCS was estimated to be 0.5 g/kg in males and more than 0.6 g/kg in females.

The objective of the present study was to determine the maximum dose of resistant maltodextrin (Fibersol)-2, a non-viscous water-soluble dietary fiber), that does not induce transitory diarrhea. Ten healthy adult subjects (5 men and 5 women) ingested Fibersol-2 at increasing dose levels of 0.7, 0.8, 0.9, 1.0, and 1.1 g/kg body weight (bw). Each administration was separated from the previous dose by an interval of 1 wk. The highest dose level that did not cause diarrhea in any subject was regarded as the maximum non-effective level for a single dose. The results showed that no subject of either sex experienced diarrhea at dose levels of 0.7, 0.8, 0.9, or 1.0 g/kg bw. At the highest dose level of 1.1 g/kg bw, no female subject experienced diarrhea, whereas 1 male subject developed diarrhea with muddy stools 2 h after ingestion of the test substance. Consequently, the maximum non-effective level for a single dose of the resistant maltodextrin Fibersol-2 is 1.0 g/kg bw for men and >1.1 g/kg bw for women. Gastrointestinal symptoms were gurgling sounds in 4 subjects (7 events) and flatus in 5 subjects (9 events), although no association with dose level was observed. These symptoms were mild and transient and resolved without treatment.

Resistant maltodextrin (RMD) is a soluble dietary fiber ingredient whose physiological functions are well recognized in Foods for Specified Health Use (FOSHU) for maintaining healthy intestinal regularity, blood glucose levels, and serum lipids. However, its efficacy on combined health risks--metabolic syndrome--was not studied yet. In this study the efficacy of RMD on humans with metabolic syndrome was investigated. A randomized double-blind placebo-controlled parallel-group trial was conducted. Thirty subjects with metabolic syndrome were randomly allocated into 2 groups and took either tea containing 9 g of RMD (treatment group) or placebo tea at three mealtimes daily for 12 wk. Blood was collected and body fat was scanned periodically. In the RMD treatment group, waist circumference, visceral fat area, fasting blood glucose, HOMA-R and serum triacylglycerol (TG) were significantly decreased compared to baseline, and significant time-by-treatment interaction was observed for waist circumference, visceral fat area, HOMA-R and serum TG (p=0.044, p=0.012, p=0.032, and p=0.049, respectively). The change ratio of visceral fat area showed negative statistical correlation with the baseline value (p=0.033), suggesting that efficacy of RMD was emphasized in the subjects having a larger visceral fat area. After the 12-wk RMD treatment, the total number of metabolic syndrome risk factors decreased to 20 from 32 with 2 subjects having no risks, while that of the placebo group decreased to 25 from 32. These findings suggest that continuous ingestion of RMD may improve the risk factors of metabolic syndrome by reducing visceral fat and improving glucose and lipid metabolism.

To examine the effects of sodium propionate on serum cholesterol levels, rats were given sodium propionate intravenously and intraperitonealy. Six-week-old male Sprague-Dawley rats were kept on a cholesterol-free semisynthetic diet for 2 weeks, fasted, and given 400 microliters of saline solution intravenously supplemented with 0.01-10 mg sodium propionate. Three hours after injection of 1 mg of sodium propionate, the serum total-cholesterol level was significantly reduced (85.4 +/- 4.0 mg/dl) compared with its starting level (102 +/- 3.4 mg/dl), with the reducing effect lasting for 24 h. The intensity of the reduction increased proportionately with increased sodium propionate concentrations from 0.01 to 1 mg. Next, to evaluate the influence of continual sodium propionate administration on serum cholesterol levels, 6-week-old male rats were implanted with an osmotic pump intraperitonealy (ALZET Model 2ML2, pumping rate: 5.0 microliter/h; duration: 14 days; reservoir volume: 2,000 microliters). At day 14, serum total-cholesterol levels were reduced by continual sodium propionate administration at both 0.12 and 1.2 mg/day. The maximum percentage change in the serum total-cholesterol level was 78.5 +/- 6.7% of its starting level (111 +/- 7.1 mg/dl), observed at 1.2 mg/day at day 7. These results indicate that sodium propionate can reduce serum total-cholesterol levels in vivo.

Hydrogenated resistant maltodextrin (H-RMD) is a dietary fiber whose energy value has not previously been reported. We evaluated the energy value of H-RMD. We conducted an in vitro digestion test, in vivo blood glucose measurement after ingestion, in vitro fermentability test, excretion test by rats and indirect calorimetry combined with breath hydrogen measurement for humans. H-RMD was hydrolyzed in vitro in a very small amount by human salivary amylase and by the rat small intestinal mucosal enzyme. Ingestion of H-RMD did not increase the blood glucose level of human subjects. An examination of in vitro fermentability suggested that H-RMD was fermented by several enterobacteria. Oral administration of H-RMD showed a saccharide excretion ratio of 42% by rats. A combination of indirect calorimetry and breath hydrogen measurement evaluated the metabolizable energy of H-RMD as 1.1 kcal/g in humans. We concluded from these results that H-RMD was not digested or absorbed in the upper gastrointestinal tract and was fermented in the colon to produce short-chain fatty acids which provided a lower amount of energy than that of resistant maltodextrin.

An examination was conducted to verify D-psicose suppressed the elevation of blood glucose and insulin concentration in a dose-dependent manner under the concurrent administration of maltodextrin and D-psicose to healthy humans. Twenty subjects aged 20-39 y, 11 males and 9 females were recruited. A load test of oral maltodextrin was conducted as a randomized single blind study. The subjects took one of five test beverages (7.5 g D-psicose alone, 75 g maltodextrin alone, 75 g maltodextrin +2.5, 5 or 7.5 g D-psicose). Blood was collected before an intake and at 30, 60, 90 and 120 min after an intake. Intervals of administration were at least 1 wk. The load test with 75 g maltodextrin showed significant suppressions of the elevation of blood glucose and insulin concentration under the doses of 5 g or more D-psicose with dose dependency. An independent administration of 7.5 g D-psicose had no influence on blood glucose or insulin concentration. D-Psicose is considered efficacious in the suppression of the elevation of blood glucose concentration after eating in humans.

The cortical innervation pattern of rat thalamic ventrolateral (VL) fibers was investigated with the Phaseolus vulgaris-leukoagglutinin (PHA-L) anterograde labeling method. The PHA-L-labeled terminals were distributed in the sensorimotor cortex where the cerebello-cerebral (C-C) evoked responses were recognized. The labeled terminals were detected in all layers except layer VI. In the upper part of layer I, the most densely packed terminals were formed and moderately labeled terminals were seen in layers IV and V. Such a laminar distribution of PHA-L-labeled VL terminals is consistent with the profiles of the C-C responses according to laminar field potential analysis.

As the physiological functions of soluble dietary fibre, the favourable efficacy, such as attenuating the absorption of saccharides or lipids, is expected. Resistant maltodextrin, a soluble dietary fibre, was investigated and found that it delays the glucose absorption and attenuates the postprandial rise in the blood glucose levels, however, the efficacy of resistant maltodextrin on lipid metabolism is not yet reported. We conducted an animal experiment and a human experiment to investigate the effect of resistant maltodextrin on postprandial blood triacylglycerol elevation. 1. Rats were fed corn oil with or without resistant maltodextrin and the postprandial changes in triacylglycerol were examined. 2. We then conducted a dietary loading experiment on 13 healthy adult male and female subjects using a meal containing approximately 50 g fat. A beverage not containing resistant maltodextrin was used as a placebo; subjects consumed the loading meal and a beverage containing either 5 g or 10 g resistant maltodextrin; blood was periodically collected to see the changes in serum constituents. 1. The corn oil administration experiment using rats showed that resistant maltodextrin dose-dependently suppressed elevation of blood triacylglycerol levels after corn oil administration. 2. The dietary loading experiment on 13 healthy subjects with 5 or 10 g of resistant maltodextrin showed that; in each administration group, resistant maltodextrin significantly suppressed postprandial elevation of blood triacylglycerol, RLP-cholesterol and insulin. These results indicate that resistant maltodextrin ingested with fatty meals suppresses the postprandial elevation of blood triacylglycerol levels.

Thalamo-parietal fibers originating from the ventroanterior-ventrolateral (VA-VL) complex in the cat were labeled with Phaseolus vulgaris leucoagglutinin (PHA-L) and examined by light and electron microscopy. PHA-L (2.5% aqueous solution) was injected iontophoretically through micropipets with anodal current pulses into the VA-VL complex. PHA-L-labeled terminals were distributed in the lateral and the suprasylvian gyri in the superficial and deep cortical layers. In layer I, horizontal varicose fibers and terminals were conspicuous in the upper one-third and were widely distributed. In the deeper cortical layers (layers III–V), varicose fibers and terminals were detected in moderate numbers. Electron microscopic examination revealed that the labeled terminals formed asymmetrical synapses on the dendritic spines of spiny neurons. These morphological findings appeared to be consistent with our previous intracellular recordings in this cortex.

To reveal the thalamic relay nucleus of the cerebellocerebral responses in the frontal association cortex, simultaneous labeling of the cerebellothalamic (C-T) terminals and the thalamocortical (T-Cx) neurons was performed in three monkeys. Horseradish peroxidase (HRP) was injected into the deep cerebellar nuclei and small doses of HRP or fluorescent dye were injected into the prefrontal cortex. The distribution of anterogradely labeled C-T terminals and retrogradely labeled T-Cx neurons was examined in the same sections. In addition to being distributed in the ventral thalamic nuclei and nucleus X, as previously reported, anterogradely labeled terminals were distributed in the ventrolateral part of the medial dorsal (MD) nucleus where retrogradely labeled thalamo-frontal projection neurons were localized. This study revealed that the ventrolateral parts of the MD together (MDmf, MDpc and MDdc) form one of the thalamic relays of the cerebelloprefrontal responses.

Intracellular recordings from thalamic neurons receiving cerebellar inputs were performed under urethane anesthesia in the rat. A total of 64 neurons were recorded intracellularly with micropipettes filled with 4% biocytin solution (dissolved in 0.5 M K-acetate), and cerebellar-induced EPSPs (CN-EPSPs), the membrane resistance and firing properties were analyzed with intracellular current injections. The mean latency of CN-EPSPs was 1.9 +/- 0.8 ms and the mean input resistance measured in 10 neurons was 17.6 +/- 5.0 M omega. Thirty-two out of 35 stained neurons were analysed morphologically; 28 of these neurons were located in the VL, and 26 received CN-EPSPs. Their somata were round or polygonal in shape and the mean size was 22.5 x 15.2 microns. They had radially extending spinous dendrites, and the mean radii of the dendritic fields were 214.7 microns in the frontal and 171.4 microns in the sagittal planes. These morphological features were similar to those observed in the sensory relay nucleus of the thalamus.