We investigated the effect of low molecular weight barley β-glucan (LMW-BG) on cecal fermentation, glucose, and lipid metabolism through comparisons to high molecular weight β-glucan (HMW-BG). C57BL/6J male mice were fed a moderate-fat diet for 61 days. LMW-BG or HMW-BG was added to the diet corresponding to 4% β-glucan. We measured the apparent absorption of fat, serum biomarkers, the expression levels of genes involved in glucose and lipid metabolism in the liver and ileum, and bacterial counts of the major microbiota groups using real time PCR. The concentration of short-chain fatty acids (SCFAs) in the cecum was analyzed by GC/MS. Significant reductions in serum leptin, total- and LDL-cholesterol concentrations, and mRNA expression levels of sterol regulatory element-binding protein-1c (SREBP-1c) were observed in both BG groups. HMW-BG specific effects were observed in inhibiting fat absorption and reducing abdominal deposit fat, whereas LMW-BG specific effects were observed in increasing bacterial counts of Bifidobacterium and Bacteroides and cecal total SCFAs, acetate, and propionate. mRNA expression of neurogenin 3 was increased in the LMW-BG group. We report that LMW-BG affects glucose and lipid metabolism via a prebiotic effect, whereas the high viscosity of HMW-BG in the digestive tract is responsible for its specific effects.

Barley is rich in soluble dietary fiber including β-glucan and arabinoxylan. Barley β-glucan is fermented by gut bacteria and, thereby contributes to an effect on intestinal bacterial composition and short-chain fatty acids (SCFAs). It also increases GLP-1 secretion via SCFAs receptor. However, few studies have focused on barley arabinoxylan. Therefore, we have investigated the effects of arabinoxylan from barley on intestinal fermentability and GLP-1 secretion. C57BL/6J mice were fed a high-fat diet containing arabinoxylan-dominant barley flour without β-glucan (bgl) and high β-glucan-containing barley flour (BF) for 12 weeks. We conducted oral glucose tolerance test (OGTT) to measure insulin and GLP-1 concentrations. The concentration of SCFAs in the cecum contents was also determined. Furthermore, we measured mRNA expression assay GLP-1 secretion using real-time PCR. The OGTT result showed that GLP-1 concentrations at 60 min were increased in mice fed bgl and BF. Acetic acid and total SCFAs concentrations in the cecum contents were increased in both the barley groups, and butyric acid was increased in the bgl group. Furthermore, the bgl and BF groups had increased Gpr43, a receptor for SCFAs, and NeuroD which is involved in L cell differentiation. These results show arabinoxylan as well as β-glucan is involved in the SCFAs-mediated increase in GLP-1 secretion upon barley consumption.

We evaluated whether intake of β-glucan-rich barley flour affects expression levels of genes related to glucose and lipid metabolism in the ileum, liver, and adipose tissues of mice fed a high-fat diet. C57BL/6J male mice were fed a high-fat diet supplemented with high β-glucan barley, for 92 days. We measured the expression levels of genes involved in glucose and lipid metabolism in the ileum, liver, and adipose tissues using DNA microarray and q-PCR. The concentration of short-chain fatty acids (SCFAs) in the cecum was analyzed by GC/MS. The metabolic syndrome indices were improved by barley flour intake. Microarray analysis showed that the expression of genes related to steroid synthesis was consistently decreased in the liver and adipose tissues. The expression of genes involved in glucose metabolism did not change in these organs. In liver, a negative correlation was showed between some SCFAs and the expression levels of mRNA related to lipid synthesis and degradation. Barley flour affects lipid metabolism at the gene expression levels in both liver and adipose tissues. We suggest that SCFAs are associated with changes in the expression levels of genes related to lipid metabolism in the liver and adipose tissues, which affect lipid accumulation.

The prebiotic effect of high β-glucan barley (HGB) flour on the innate immune system of high-fat model mice was investigated. C57BL/6J male mice were fed a high-fat diet supplemented with HGB flour for 90 days. Secretory immunoglobulin A (sIgA) in the cecum and serum were analyzed by enzyme-linked immunosorbent assays (ELISA). Real-time PCR was used to determine mRNA expression levels of pro- and anti-inflammatory cytokines such as interleukin (IL)-10 and IL-6 in the ileum as well as the composition of the microbiota in the cecum. Concentrations of short-chain fatty acids (SCFAs) and organic acids were analyzed by GC/MS. Concentrations of sIgA in the cecum and serum were increased in the HGB group compared to the control. Gene expression levels of IL-10 and polymeric immunoglobulin receptor (pIgR) significantly increased in the HGB group. HGB intake increased the bacterial count of microbiota, such as Bifidobacterium and Lactobacillus. Concentrations of propionate and lactate in the cecum were increased in the HGB group, and a positive correlation was found between these organic acids and the IL-10 expression level. Our findings showed that HGB flour enhanced immune function such as IgA secretion and IL-10 expression, even when the immune system was deteriorated by a high-fat diet. Moreover, we found that HGB flour modulated the gut microbiota, which increased the concentration of SCFAs, thereby stimulating the immune system.

Barley is rich in β-glucan, which can alter gut microbiota and metabolome profiles, potentially affecting host metabolism. However, the microbiota and metabolites increased by barley β-glucan remain unclear. In this study, we focused on the gut-microbiota-derived metabolite succinate and investigated the microbiome and metabolome profiles altered by barley β-glucan intake. C57BL/6 J mice were fed a standard or middle-fat diet containing barley flour rich in β-glucan or barley flour without β-glucan, and their gut microbiota and metabolome profiles were analyzed. The results showed increased Bacteroides, Parasutterella, and succinate due to barley β-glucan intake independent of diet differences. Next, we used mice lacking slc13a2, a gene that is involved in the cellular uptake of succinate. Wild-type mice showed improved glucose tolerance after the intake of barley β-glucan, but this effect was attenuated in the slc13a2-deficient mice. These results suggest that barley β-glucan intake increases succinate and succinate-producing bacteria and affects glucose metabolism.