This increase was most obvious in the treatment with 0.9% of H2O2/30 min, 0.6% and 0.9% of H2O2/60 min, with values up to 10 times higher than those of native β-glucan (4.09 mg/dL LDN 193189 in native β-glucan versus 52.73 mg/dL in β-glucan treated with 0.9% of H2O2/30 min; Table 2). This behaviour is probably due to the depolymerisation of the molecule caused by the action of hydrogen peroxide, similar to what occurs in other polysaccharides, such as starch, alginate and chitosan ( Li et al., 2010, Sangseethong et al., 2010 and Tian et al., 2004). Part of that increase can also be a function of depolymerisation of residual starch in the β-glucan concentrate. Depolymerisation increases the carbohydrate molecule’s

susceptibility to chemical action, which can increase the postprandial blood glucose. Moreover, the increase in available glucose after chemical digestion indicates that oxidised β-glucan is more susceptible to stomach acids, and this degradation of the molecule can decrease biological activity in the intestines. The oxidative treatment did not affect the fat binding of β-glucan, with 3.97 g oil/g sample of fat binding PCI-32765 nmr found among the treatments (Table 2). The in-vitro studies of Bae et al. (2009), using hydrolysed β-glucan from oats with different molecular weights, found that

the fat-binding values varied between 3.9 and 11.4 g oil/g sample, with 3.9 g oil/g sample found in unhydrolysed β-glucan. Bile acid is synthesised from cholesterol in the liver. β-Glucan can bind bile acid in the intestine, thus increasing faecal bile acid excretion and tending to lower cholesterol in the blood (Bae et al., 2009). Oxidative treatment with hydrogen peroxide increased the bile acid-binding Selleck Afatinib of the β-glucan. Bile acid binding ranged from 11.33% in native β-glucan to 16.06% in the treatment with 0.9% of H2O2/30 min, with the exception of the treatment

with less oxidative intensity (0.3% of H2O2/30 min), which exhibited 11.29% of bile acid binding (Table 2). Bae et al. (2009), in a study of β-glucan concentrates from oats of 43% purity, found 13.1% bile acid binding in native β-glucan; however, after hydrolysis, the bile acid binding ranged between 6.4% and 26.5%. According to these authors, several factors influence the bile acid binding of β-glucan, such as structural and physicochemical properties and molecular weight. Yao, White, Jannink, and Alavi (2008) in a study with extruded oat cereals, processed from two oat lines with β-glucan concentrations of 8.7 and 4.9%, suggest the importance of considering not only the absolute amount of β-glucan intake but also the viscosity caused by the β-glucan in the food consumed, when evaluating the impact on bile acid binding. The minimum amount of β-glucan concentrate necessary to form a strong gel (i.e., one that did not fall out or slip down the sides inverted test tubes) was 12%.