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.

Preliminary genome-wide association study of bipolar disorder in the Japanese population.

Recent progress in genotyping technology and the development of public databases has enabled large-scale genome-wide association tests with diseases. We performed a two-stage genome-wide association study (GWAS) of bipolar disorder (BD) in Japanese cohorts. First we used Affymetrix 100K GeneChip arrays in the analysis of 107 cases with bipolar I disorder and 107 controls, and selected markers that were nominally significant (P < 0.01) in at least one of the three models (1,577 markers in total). In the follow-up stage, we analyzed these markers using an Illumina platform (1,526 markers; 51 markers were not designable for the platform) and an independent sample set, which consisted of 395 cases (bipolar I + II) and 409 controls. We also assessed the population stratification of current samples using principal components analysis. After the two-stage analysis, 89 markers remained nominally significant (allelic P < 0.05) with the same allele being consistently over-represented in both the first and the follow-up stages. However, none of these were significant after correction for multiple-testing by false discovery rates. Sample stratification was virtually negligible. Collectively, this is the first GWAS of BD in the Japanese population. But given the small sample size and the limited genomic coverage, these results should be taken as preliminary.

Impairment of theory of mind in patients in remission following first episode of schizophrenia.

The aim of this study was to investigate theory of mind (ToM) ability in patients in remission after the first episode of schizophrenia. A ToM task which contained four pictures was given to 30 patients with schizophrenia in remission and 30 matched healthy controls. Patients with schizophrenia in remission showed statistically significant impairment in the ToM tasks. ToM impairment was not correlated with psychiatric symptoms. Thus, ToM deficit in schizophrenia may be a trait marker.

Eating disorders with binge-eating behaviour are associated with the s allele of the 3'-UTR VNTR polymorphism of the dopamine transporter gene.

OBJECTIVE: The dopaminergic system is associated with feelings of pleasure and reward and with positive hedonic processes related to food, sexual activity and certain substances. Because it is recognized that patients who have eating disorders with binge-eating behaviour have a high comorbidity of substance dependence, we examined the association between the variable number of tandem repeats (VNTR) polymorphism in the 3; untranslated region of the dopamine transporter gene (DAT1) and eating disorders with binge-eating behaviour. METHODS: The subjects were 90 female Japanese patients with eating disorders diagnosed using DSM-IV; they were compared with 115 healthy female controls. Genomic DNA was extracted from whole blood, and standard polymerase chain reaction testing was performed. We compared the frequencies of a short allele (7 or 9 repeats) and a long allele (10 or 11 repeats) in both groups. RESULTS: In the group who had an eating disorder with binge-eating behaviour, the frequency of a short allele was significantly higher compared with the control group. CONCLUSION: It seems plausible that the association between the DAT1 VNTR and binge-eating behaviour indicates that dysregulation of dopamine reuptake may act as a common pathophysiologic mechanism in eating disorders with binge-eating behaviour and in disorders related to substance use.

No association between genotype of the promoter region of serotonin transporter gene and serotonin transporter binding in human brain measured by PET.

The human serotonin transporter (5-HTT) gene has a polymorphism in the 5'-flanking promoter region that is called the serotonin transporter gene-linked polymorphic region (5-HTTLPR). In lymphoblast cell lines, the promoter activity of the 5-HTT gene is dependent on 5-HTTLPR allelic variants. The transcriptional activity of the l allele was more than twice as high as that of the s allele. The s allele is considered to be associated with mood disorders and anxiety-related personality traits. To evaluate the functional differences of 5-HTTLPR in the brain in vivo, we examined the allelic variations of 5-HTTLPR and measured 5-HTT binding in the living human brain using positron emission tomography (PET) with C(11)-labeled trans-1, 2, 4, 5, 6, 10-beta-hexahydro-6-[4-(methylthio) phenyl]pyrrolo[2,1-a]isoquinoline (McN5652) as a ligand. Twenty-seven healthy male subjects participated in this study. Although the human lymphoblast cells with the l/l genotype was reported to produce higher concentrations of both mRNA and protein of 5-HTT than those with the l/s or s/s genotype in a human lymphoblast in vitro study, 5-HTT binding in vivo was not significantly different among subjects with the three genotypes (l/l: 0.842 +/- 0.184, l/s: 0.708 +/- 0.118, s/s: 0.825 +/- 0.209). In conclusion, this study does not support the assumption that the genotype-dependent differences of 5-HTTLPR directly contributes to the regulation of the 5-HTT binding site in the living human brain.

The genetic structure of Cloninger's seven-factor model of temperament and character in a Japanese sample.

Theoretical assumptions regarding the genetic and environmental structure of personality proposed in Cloninger's seven-factor model of temperament and character were verified in a Japanese sample by using the twin method. The Temperament and Character Inventory (TCI) was administered to 296 twin pairs ranging in age from 14 to 28 years old. Among four temperament dimensions (novelty seeking [NS], harm avoidance [HA], reward dependence [RD], and persistence [PS]), HA and PS showed significant additive genetic contributions and no shared environmental effect, supporting the original theoretical assumption. NS and RD could be explained by either genetic or shared environmental factors with nonshared environment. All three character dimensions (cooperativeness [CO], self-directedness [SD], and self-transcendence [ST]) could be explained exclusively by additive contributions and no shared environmental effect. Multivariate genetic analysis indicated that there were no significant associations between NS, HA, and RD, as the theory predicts, and the genetic components of PS, SD, and CO were derived from those of the temperament dimensions. The fourth genetic component, which had a substantial load specifically on ST and overlapped with PS, was identified. Although most of the nonshared environmental effects were trait-specific, the phenotypic correlation between NS and HA could be explained by nonshared environmental overlap.