Effect of High ß-Glucan Barley on Postprandial Plasma Glucose Levels in Subjects with Normal Glucose Tolerance and Patients with Type 2 Diabetes

Abstract

Increasing evidence supports a more prominent role for postprandial glucose (PPG) regulation in the management of type 2 diabetes. Viscous dietary fibers including oat and barley β-glucan are one of the most effective classes of functional food ingredients for reducing PPG. We investigated the effect of high β-glucan barley on postprandial plasma glucose and C-peptide levels using a meal tolerance test and continuous glucose monitoring (CGM) in 15 subjects with normal glucose tolerance (NGT) and 29 type 2 diabetic patients. A 500-kcal meal tolerance test, using white rice alone (white rice) or white rice mixed with 50% of barley (Kirari-mochi®) containing 1.5-times β-glucan higher than usual barley (barley), was performed, and plasma glucose and C-peptide levels were measured every 30 minutes for 180 minutes. Daily glucose variability was measured using CGM over two days, while subjects consumed 1600-kcal or 1800-kcal test meals consisting of white rice or barley. Subsequently, a meal tolerance test with identical carbohydrate quantity (52g carbohydrate) with or without 1.8g of β-glucan, was performed in 7 diabetic patients. In NGT subjects and diabetic patients, the incremental area under the curve (AUC) of plasma glucose and C-peptide levels for 180 minutes after the meal tolerance test were significantly decreased following the consumption of barley compared to the consumption of white rice alone. The studies using CGM have demonstrated that the consumption of barley lead to a significant decrease in the 24-h standard deviation of blood glucose (24-h SDBG) and mean amplitude of glycemic excursion (MAGE) in diabetic patients. Similar results were obtained in subsequent tests with identical carbohydrate quantity but with β-glucan. In conclusion, these results suggest that high-β-glucan barley may contribute to decreased PPG levels and endogenous insulin secretion in both patients with type 2 diabetes and the subjects with NGT. Disclosure M. Higa: None. A. Hashimoto: None. M. Hayasaka: None. M. Hijikata: None. A. Ueda: None. K. Oda: None. D. Kato: None. K. Yamashita: None. T. Ichijo: None.