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Recent researches have revealed an association between circulating branched-chain acid (BCAA) and obesity and insulin resistance. In addition, experiments using rodents have revealed that adiponectin (APN) regulates the systemic BCAA level by affecting its catabolism. However, the influence of glucose intolerance on the relationship between BCAA and insulin sensitivity (IS) and between APN and BCAA in humans is unknown. Hence, we aimed to investigate these associations in individuals with varying degrees of glucose tolerance. Based on the data of 75g OGTT in 75 Japanese individuals without diabetic medication [age:65±11 (mean±SD); BMI: 24.9±3.8], individuals were classified into the normal, impaired glucose tolerance, and diabetes (DM) group (n=25 in each group). Matsuda index (MI) was calculated as an index of IS. Normally-distributed loge-transformed (ln-) values were used for MI and APN. Fasting BCAA was assayed using an enzymatic method. In analysis of total individuals using stepwise regression analysis, BMI (β=-0.477, p Disclosure E. Amano: None. K. Yoshimura: None. S. Funakoshi: None. S. Hirano: None. S. Ohmi: None. Y. Terada: None. S. Fujimoto: None.

Aims/Introduction Mannose is a monosaccharide constituent of glycoproteins and glycolipids. Experiments in rats have shown previously that the plasma mannose level decreases after glucose load, but does not decrease in diabetic rats, and that hepatic glycogenolysis is a source of this plasma mannose; however, these results are not fully elucidated in humans. Plasma mannose levels before/after glucose loading in humans with various degrees of glucose intolerance were examined to analyze their association with clinical factors. Materials and Methods The 75-g oral glucose tolerance test was carried out in Japanese individuals not taking diabetes medications. Participants were classified into normal glucose tolerance, impaired glucose metabolism and diabetes mellitus groups. Insulinogenic index as an index of insulin secretion, and Matsuda Index as an index of insulin sensitivity were calculated. Mannose was assayed by the established method using high-performance liquid chromatography after labeling. Results After glucose load, the plasma mannose level decreased gradually in the normal glucose tolerance group, but did not decrease in the diabetes mellitus group. Plasma mannose changes during 120 min from baseline (M120-M0) were significantly different among the three groups (normal glucose tolerance: −16.7 ± 1.7; impaired glucose metabolism: −9.0 ± 1.9; diabetes mellitus: −1.4 ± 1.8 μmol/L [n = 25 in each group], P

Background Recently, an integrated network analysis has revealed dysregulation in the metabolism of mannose, a glucose epimer, in severely obese individuals without diabetes. In addition, fasting plasma mannose levels (M0) are associated with insulin resistance independent of BMI. Since the association between mannose and insulin sensitivity (IS) in those with impaired glucose tolerance remains unknown, we aimed to investigate this association in individuals without severe obesity but with varying degrees of glucose tolerance. Methods Based on 75 g OGTT data in Japanese individuals without diabetic medication, individuals were classified as having normal glucose tolerance (NGT), impaired glucose metabolism (IGM), or diabetes (DM). In each group, 25 individuals were consecutively recruited [total 75 individuals, age: 65 ± 11 (mean ± SD); BMI: 24.9 ± 3.8 kg/m2]. QUICKI and Matsuda index (MI) were calculated as IS indices. M0 was assayed using HPLC. Normally-distributed loge-transformed (ln-) values were used for MI and leptin. Results In the simple regression analysis, ln-MI was negatively correlated with BMI (NGT: r = − 0.639, IGM: r = − 0.466, DM: r = − 0.613) and ln-leptin (NGT: r = − 0.480, IGT: r = − 0.447, DM: r = − 0.593) in all 3 groups. Ln-MI was not significantly correlated with M0 in NGT (r = 0.241, P = 0.245) and IGT (r = − 0.296, P = 0.152) groups, it was moderately and negatively correlated in the DM group (r = − 0.626, P

Recently, integrated network analysis has revealed dysregulation in the metabolism of mannose, an epimer of glucose, in individuals with severe obesity who do not have significant diabetes. It was also found that fasting plasma mannose levels (M0) are associated with insulin resistance independent of BMI. Since the association between mannose and insulin sensitivity (IS) in those with impaired glucose tolerance remains unknown, we aimed to investigate the association in individuals with varying degrees of glucose tolerance. Based on data of 75g OGTT in Japanese individuals without diabetic medication, individuals were classified as normal (NGT), impaired glucose tolerance (IGT), and diabetes (DM). In each group, 25 subjects were consecutively recruited [total 75 individuals, age: 65±11 (mean±SD); BMI: 24.9±3.8]. Matsuda index (MI) was calculated as an index of IS. M0 was assayed using HPLC. Normally-distributed loge-transformed (ln-) values were used for MI and leptin. Although fasting plasma glucose (G0), HbA1c, and ln-MI were significantly different among 3 groups, age, sex, BMI, and M0 were not different. In simple regression analysis, ln-MI was negatively correlated with BMI (NGT: r=-0.639, IGT: r=-0.466, DM: r=-0.613) and ln-leptin (NGT: r=-0.480, IGT: r=-0.447, DM: r=-0.593) in all 3 groups. Interestingly, although ln-MI was not significantly correlated with M0 in NGT (r=0.241, P=0.245) and IGT (r=-0.296, P=0.152), it was moderately and negatively correlated in DM (r=-0.626, P In conclusion, in our study, fasting plasma mannose was associated with insulin sensitivity independent of BMI in Japanese individuals with diabetes. Disclosure E. Amano: None. S. Funakoshi: None. K. Yoshimura: None. S. Hirano: None. S. Ohmi: None. Y. Terada: None. S. Fujimoto: None.

Background While the association of the prevalence of non-alcoholic fatty liver disease (NAFLD) with impaired glucose metabolism has been reported, the factors influencing glucose tolerance in NAFLD remain to be clarified. Methods Glucose tolerance of 131 Japanese patients diagnosed as NAFLD by histological findings of liver biopsy specimen was examined using 75 g-OGTT. According to Matteoni’s classification, patients were divided to 4 groups [M1 ~ 4, M1, 2: non-alcoholic fatty liver (NAFL); and M3, 4: non-alcoholic steatohepatitis (NASH)]. Based on the OGTT data, insulinogenic index (IGI) and QUICKI were calculated as indices of insulin secretion and insulin sensitivity, respectively. Plasma glucose 120 min after glucose loading (G120) was used as the index for glucose intolerance. Results Stepwise multiple regression analysis using G120 as a dependent variable and loge-IGI, QUICKI, sex, BMI, age, NAFL/NASH as independent variables revealed that loge-IGI (β = −0.595) and QUICKI (β = −0.323) are significant factors predicting glucose intolerance (R2 = 0.403), indicating an important role of insulin secretion in glucose tolerance. These findings accord with glucose intolerance as high as 89.7% in patients with impaired insulin secretion defined by ≤43.2 pmol/mmol (40 μU/mg) IGI. Stepwise multiple regression analysis using QUICKI as a dependent variable and NAFL/NAFLD, sex, BMI, and age as independent variables revealed that BMI (β = −0.469) and NAFL/NAFLD (β = −0.204) are significant factors predicting insulin sensitivity (R2 = 0.248). Conclusion Impairment of insulin secretion is the most important factor to predict glucose intolerance in NAFLD; severity of histological findings is associated with insulin sensitivity independent of adiposity in NAFLD.

We evaluated the neural substrates of cross-modal binding and divided attention during audio-visual speech integration using functional magnetic resonance imaging. The subjects (n = 17) were exposed to phonemically concordant or discordant auditory and visual speech stimuli. Three different matching tasks were performed: auditory-auditory (AA), visual-visual (VV) and auditory-visual (AV). Subjects were asked whether the prompted pair were congruent or not. We defined the neural substrates for the within-modal matching tasks by VV-AA and AA-VV. We defined the cross-modal area as the intersection of the loci defined by AV-AA and AV-VV. The auditory task activated the bilateral anterior superior temporal gyrus and superior temporal sulcus, the left planum temporale and left lingual gyrus. The visual task activated the bilateral middle and inferior frontal gyrus, right occipito-temporal junction, intraparietal sulcus and left cerebellum. The bilateral dorsal premotor cortex, posterior parietal cortex (including the bilateral superior parietal lobule and the left intraparietal sulcus) and right cerebellum showed more prominent activation during AV compared with AA and VV. Within these areas, the posterior parietal cortex showed more activation during concordant than discordant stimuli, and hence was related to cross-modal binding. Our results indicate a close relationship between cross-modal attentional control and cross-modal binding during speech reading.