Abstract
The cholesterol-lowering effect observed following consumption of oats and barley is attributable to the β-glucan component of the soluble fiber fraction of these cereal grains. β-Glucan has also been reported to modulate immune activity, however, few studies have evaluated the hematological effects of β-glucan following oral exposure. In the current study, a concentrated β-glucan (64%) preparation from barley (Barley Betafiber) was blended into mouse feed at concentrations of 1, 5, or 10% (corresponding to approximately 0.7, 3.5, and 7% β-glucan) and evaluated in CD-1 mice. Plasma was collected for clinical chemistry and hematological measurements at the initiation of the study and again following 14 and 28 days of exposure. Plasma was also collected from animals that consumed the same diets for 28-days but were switched to control diet (containing no supplemental β-glucan) for an additional 14-day period to evaluate reversibility or delayed occurrence of treatment-related changes. Half of the animals were sacrificed for histopathologic analysis following the 28-day exposure period and the other half were evaluated following the recovery period. Histopathologic analysis focused on primary lymphoid organs and lymph nodes proximal and distal to the route of exposure. An additional group of untreated animals (naı̈ve) was bled and sacrificed at day 0, 14, 27 and 41 for comparison of the hematology parameters with those of the control group because it was not known if multiple blood draws would affect hematology parameters. Compared to animals consuming the control diet, no treatment-related adverse effects were observed in hematological or clinical chemistry measurements or in organ weights and immunopathology in either sex following consumption of concentrated barley β-glucan for 28-days or following the recovery period. Likewise, no differences were observed between the naı̈ve and control groups. Results from this study showed that consumption of concentrated barley β-glucan did not cause treatment-related inflammatory or other adverse effects in CD-1 mice.
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