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Oats contain a range of phenolic acids and avenanthramides which may have health benefits. Analysis of 22 commercial oat products (oat bran concentrate, oat bran, flaked oats, rolled oats and oatcakes) using HPLC-DAD detected eleven bound and thirteen free + conjugated phenolic acids and avenanthramides. The oat products (excluding concentrate) provided between 15.79 and 25.05 mg total phenolic acids (9.9-19.33 mg bound, 4.96-5.72 mg free + conjugated) and between 1.1 and 2 mg of avenanthramides in a 40 g portion while an 11 g portion of oat concentrate provided 16.7 mg of total phenolic acids (15.17 mg bound, 1.53 mg free + conjugated) and 1.2 mg of avenanthramides. The compositions and concentrations of the components in the different products were broadly similar, with the major component being ferulic acid (58-78.1%). The results show that commercial oat products are a source of phenolic acids and avenanthramides for consumers.

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Wholegrain oats are known to modulate the human gut microbiota and have prebiotic properties (increase the growth of some health-promoting bacterial genera within the colon). Research to date mainly attributes these effects to the fibre content; however, oat is also a rich dietary source of polyphenols, which may contribute to the positive modulation of gut microbiota. In vitro anaerobic batch-culture experiments were performed over 24 h to evaluate the impact of two different doses (1 and 3 % (w/v)) of oat bran, matched concentrations of ß-glucan extract or polyphenol mix, on the human faecal microbiota composition using 16S RNA gene sequencing and SCFA analysis. Supplementation with oats increased the abundance of Proteobacteria (P <0·01) at 10 h, Bacteroidetes (P <0·05) at 24 h and concentrations of acetic and propionic acid increased at 10 and 24 h compared with the NC. Fermentation of the 1 % (w/v) oat bran resulted in significant increase in SCFA production at 24 h (86 (sd 27) v. 28 (sd 5) mm; P <0·05) and a bifidogenic effect, increasing the relative abundance of Bifidobacterium unassigned at 10 h and Bifidobacterium adolescentis (P <0·05) at 10 and 24 h compared with NC. Considering the ß-glucan treatment induced an increase in the phylum Bacteroidetes at 24 h, it explains the Bacteriodetes effects of oats as a food matrix. The polyphenol mix induced an increase in Enterobacteriaceae family at 24 h. In conclusion, in this study, we found that oats increased bifidobacteria, acetic acid and propionic acid, and this is mediated by the synergy of all oat compounds within the complex food matrix, rather than its main bioactive ß-glucan or polyphenols. Thus, oats as a whole food led to the greatest impact on the microbiota.

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SCOPE: Wholegrain has been associated with reduced chronic disease mortality, with oat intake particularly notable for lowering blood cholesterol and glycemia. To better understand the complex nutrient profile of oats, we studied urinary excretion of phenolic acids and avenanthramides after ingestion of oat bran in humans. METHODS AND RESULTS: After a 2-d (poly)phenol-low diet, seven healthy men provided urine 12 h before and 48 h after consuming 60 g oat bran (7.8 µmol avenanthramides, 139.2 µmol phenolic acids) or a phenolic-low (traces of phenolics) control in a crossover design. Analysis by ultra-high performance liquid chromatography (UPLC)-MS/MS showed that oat bran intake resulted in an elevation in urinary excretion of 30 phenolics relative to the control, suggesting that they are oat bran-derived. Mean excretion levels were elevated between 0-2 and 4-8 h, following oat bran intake, and amounted to a total of 33.7 ± 7.3 µmol total excretion (mean recovery: 22.9 ± 5.0%), relative to control. The predominant metabolites included: vanillic acid, 4- and 3-hydroxyhippuric acids, and sulfate-conjugates of benzoic and ferulic acids, which accounted collectively for two thirds of total excretion. CONCLUSION: Oat bran phenolics follow a relatively rapid urinary excretion, with 30 metabolites excreted within 8 h of intake. These levels of excretion suggest that bound phenolics are, in part, rapidly released by the microbiota.

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BACKGROUND: Prospective cohort studies show that higher dietary fiber intake is associated with reduced cardiovascular disease risk, yet the impact on postprandial glucose and insulin responses is unclear. OBJECTIVE: This study aims to evaluate the effects of orange beverages with differing fiber concentrations on postprandial glycemic responses (secondary outcome measure) after a sequential breakfast and lunch challenge in men with increased cardiometabolic risk. METHODS: Thirty-six men (aged 30-65 y; body mass index 25-30 kg/m(2): fasting triacylglycerol or total cholesterol concentrations: 0.8-2.2 or 6.0-8.0 mmol/L, respectively) were provided with a high-fat mixed breakfast and were randomly assigned to consume 240 mL Tropicana (PepsiCo, Inc.) pure premium orange juice without pulp (OJ), OJ with 5.5 g added orange pomace fiber (OPF), juice made from lightly blended whole orange, or an isocaloric sugar-matched control (Control) on 4 occasions separated by 2 wk. A medium-fat mixed lunch was provided at 330 min. Blood samples were collected before breakfast and on 11 subsequent occasions for 420 min (3 time points postlunch) to determine postprandial glucose, insulin, lipid, and inflammatory biomarker responses. Repeated-measures ANOVA was used for data analysis. RESULTS: OPF significantly (P < 0.05) reduced the maximal change in glucose concentrations (1.9 ± 0.21 mmol/L) reached after breakfast compared with other treatments (2.3-2.4 mmol/L) and after lunch (3.0 ± 0.05 mmol/L) compared with OJ (3.6 ± 0.05 mmol/L). The maximal change in insulin concentration (313 ± 25 pmol/L) was also lower compared with Control (387 ± 30 pmol/L) and OJ (418 ± 39 pmol/L) after breakfast. OPF significantly delayed the time to reach the peak glucose concentration compared with Control and OJ, and of insulin compared with Control after breakfast. CONCLUSION: OPF consumed with breakfast may lower postprandial glycemic and insulinemic responses to typical meal ingestion in men with increased cardiometabolic risk. This trial is registered at clinicaltrials.gov as NCT01963416.

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