Co-ingestion of traditional Japanese barley mixed rice (Mugi gohan) with yam paste in healthy Japanese adults decreases postprandial glucose and insulin secretion in a randomized crossover trial.

BACKGROUND AND OBJECTIVES: Barley mixed rice, "Mugi gohan," is traditionally eaten with yam paste in Japan. Both ingredients contain dietary fiber and reportedly reduce postprandial hyperglycemia. However, evidence supporting the benefits of combining barley mixed rice with yam paste is limited. In this study, we evaluated whether ingesting a combination of barley mixed rice and yam paste affected postprandial blood glucose concentration and insulin secretion. METHODS AND STUDY DESIGN: This study followed an open-label, randomized controlled crossover design, following the unified protocol of the Japanese Association for the Study of Glycemic Index. Fourteen healthy subjects each consumed four different test meals: white rice only, white rice with yam paste, barley mixed rice, and barley mixed rice with yam paste. We measured their postprandial blood glucose and insulin concentrations after every meal, and we calculated the area under curve for glucose and insulin. RESULTS: Participants had significantly reduced area under curve for glucose and insulin after eating barley mixed rice with yam paste compared to when they ate white rice only. Participants had similar area under curve for glucose and insulin after eating barley mixed rice only, or eating white rice with yam paste. Participants had lower blood glucose concentrations 15 min after eating barley mixed rice only, whilst eating white rice with yam paste did not maintain lower blood glucose after 15 min. CONCLUSIONS: Eating barley mixed rice with yam paste decreases postprandial blood glucose concentrations and reduces insulin secretion.

Consumption of a meal containing refined barley flour bread is associated with a lower postprandial blood glucose concentration after a second meal compared with one containing refined wheat flour bread in healthy Japanese: A randomized control trial.

OBJECTIVE: Foods reducing postprandial hyperglycemia could suppress the postprandial blood glucose response after the next meal (a "second-meal" effect). However, the second-meal effect of refined barley flour bread has not been evaluated. The aim of this study is to determine whether consumption of refined barley flour bread reduces postprandial glucose concentrations after this and the subsequent meal. METHODS: We enrolled 23 healthy young Japanese adults and conducted a randomized, double-blind, placebo-controlled, crossover study. The participants consumed refined barley flour bread containing 2.5 g ß-glucan or refined wheat flour bread in a first meal, then consumed three rice balls as a second meal. Their postprandial blood glucose concentrations were measured 0, 15, 30, 45, 60, 90, and 120 min after both meals. Participants with fasting glucose concentrations above the diagnostic threshold for diabetes were excluded. RESULTS: The blood glucose concentration 30 min after the first meal was significantly lower (P < 0.05) if refined barley flour bread (7.1 ± 1.0 mmol/L) rather than refined wheat flour bread (7.7 ± 1.2 mmol/L) was consumed. Significantly lower glucose concentrations after the second meal measured at 60 (P < 0.05, barley flour bread: 8.7 ± 1.8 mmol/L, wheat flour bread: 9.3 ± 1.7 mmol/L) and 90 min (P < 0.01, barley flour bread: 7.8 ± 1.4 mmol/L, wheat flour bread: 8.8 ± 2.1 mmol/L) were lower in participants who had previously consumed the refined barley flour bread. CONCLUSIONS: Consumption of bread made with refined barley flour lowers postprandial blood glucose concentration after this and a subsequent meal compared with the consumption of refined wheat flour bread in healthy young Japanese adults.

Dioxin-induced up-regulation of the active form of vitamin D is the main cause for its inhibitory action on osteoblast activities, leading to developmental bone toxicity.

Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is known to cause bone toxicity, particularly during animal development, although its action mechanism to cause this toxicity has yet to be elucidated. Mouse pups were exposed to TCDD via dam's milk that were administered orally with 15 microg TCDD/kg b.w. on postnatal day 1. Here we report that TCDD causes up-regulation of vitamin D 1alpha-hydroxylase in kidney, resulting in a 2-fold increase in the active form of vitamin D, 1,25-dihydroxyvitamin D3, in serum. This action of TCDD is not caused by changes in parathyroid hormone, a decrease in vitamin D degrading enzyme, vitamin D 24-hydroxylase, or alterations in serum Ca2+ concentration. Vitamin D is known to affect bone mineralization. Our data clearly show that TCDD-exposed mice exhibit a marked decrease in osteocalcin and collagen type 1 as well as alkaline phosphatase gene expression in tibia by postnatal day 21, which is accompanied with a mineralization defect in the tibia, lowered activity of osteoblastic bone formation, and an increase in fibroblastic growth factor-23, a sign of increased vitamin D effect. Despite these significant effects of TCDD on osteoblast activities, none of the markers of osteoclast activities was found to be affected. Histomorphometry confirmed that osteoblastic activity, but not bone resorption activity, was altered by TCDD. A prominent lesion commonly observed in these TCDD-treated mice was impaired bone mineralization that is characterized by an increased volume and thickness of osteoids lining both the endosteum of the cortical bone and trabeculae. Together, these data suggest that the impaired mineralization resulting from reduction of the osteoblastic activity, which is caused by TCDD-induced up-regulation of vitamin D, is responsible for its bone developmental toxicity.

Polymerizable gemini surfactants at solid/solution interfaces: adsorption and polymerization on melamine formaldehyde particles and capsule fabrication.

Organic capsules have been fabricated via three steps, by using the polymerizable gemini surfactant (1,2-bis(dimethyl(11-methacryloyloxy)undecylammonio) hexane dibromide, PC11-6-11) as a single wall component. In the first fabrication step, the surfactant spontaneously adsorbs on acid-dissolvable melamine formaldehyde (MF) particles in aqueous media. The adsorption isotherm data reveal that the adsorbed amount of PC11-6-11 (per chain) is greater than that of the corresponding monomeric surfactant ((11-methacryloyloxy)undecyltrimethylammonium bromide, PC11), resulting from the greater intermolecular association of PC11-6-11 at the solid/solution interface. The closely packed adsorbed layer of PC11-6-11 provides an opportunity to give a polymer thin film, as a result of in situ photo-polymerization on MF particles (in the second fabrication step) and subsequent acid dissolution of the core MF particles (in the third fabrication step). The dynamic light scattering (DLS) measurements have shown that the apparent hydrodynamic diameter of PC11-6-11 capsules is reversibly changed in response to a change in ionic strength: the increased background electrolyte concentration results in deswelling of the capsules, and vice versa. It seems likely that this swelling/deswelling behavior is primarily driven by the electrostatic interaction between quaternary ammonium groups within the polymerized film. We have also studied the capture and release capabilities of glucose into/from the capsule core and found that (i) glucose is encapsulated into the capsule core at high electrolyte concentrations and (ii) the glucose molecules encapsulated into the core are gradually released when the outer electrolyte solution is replaced by pure water. We believe, therefore, that the PC11-6-11 capsules fabricated here are useful as stimulus-responsive smart vehicles.

A 12-year-old boy with acute gastroenteritis caused by Edwardsiella tarda O4:H4.

A 12-year-old boy was brought to the hospital with a 3-week history of watery diarrhea mixed with mucus and colicky abdominal pain. Stool culture identified Edwardsiella tarda O4: H4, and no other pathogenic bacteria were detected. Acute gastroenteritis caused by Edwardsiella tarda O4: H4 was diagnosed. This bacterium was shown to be sensitive to ampicillin hydrate. When this antibiotic was administered, the condition of the patient improved within a week. The patient had a history of eating raw shrimp and fish while traveling with his parents.