Effect of Fiber Intake on Glycemia, Insulin Secretion, and Inflammation in Patients with Type 2 Diabetes

Abstract

Hypothesis. In view of the reduction in post prandial glucose concentrations and an increase in insulin concentrations and the inhibition of post prandial endotoxemia and increases in TLR-4 and TLR-2 expression following the intake of fiber with a high fat high calorie meal (HFHC) in normal subjects, we hypothesized that a similar effect would be observed following the intake with such a meal in patients with type 2 diabetes. Methods. Ten patients with type diabetes were included in the study and were administered the HFHC meal alone on one day and with dietary fiber (28gram of mainly insoluble fiber) a week later. Fasting premeal and post meal samples were obtained sequentially at hourly intervals for 5 hours. Blood samples were processed for preparation of peripheral blood mononuclear cells (MNC), plasma and serum. Results. Post meal glucose concentrations were not altered significantly but the peak increase in post meal insulin concentrations was greater after fiber (34±6 vs. 26±4µU/ml, p<0.01) as well as the area under curve (AUC5h) (3234±733 vs. 2214±464µU*5h*ml-1, p<0.01). Fiber intake also induced an early peak of GLP-1 within 15 minutes (29±15% over baseline, NS) which was missing without fiber. Reactive oxygen species (ROS) generation and NFκB binding by MNC was significantly suppressed after fiber by 32±11% and 38±13%, respectively (p<0.01), as was the magnitude of endotoxemia AUC5h by 23±8% (p<0.05). In addition, the increase in the expression of TLR-4 and TLR-2 was also suppressed by 42±15% and 36±14%, respectively (p<0.05) Conclusions. The intake of fiber resulted in an early peak of GLP-1 and a greater increase in insulin concentrations but the increase in glucose was not altered. Fiber intake also suppressed ROS generation and NFκB binding while reducing the magnitude of endotoxemia and the receptor to endotoxin. Thus, the intake of fiber increases insulinogenesis and reduces oxidative and inflammatory stress in patients with type 2 diabetes. Disclosure C. Tang: None. H. Ghanim: None. K. Green: None. A. Makdissi: Speaker's Bureau; Self; Eli Lilly and Company. M. Batra: Speaker's Bureau; Self; Eli Lilly and Company. A. Chaudhuri: Speaker's Bureau; Self; AstraZeneca, Eli Lilly and Company, Boehringer Ingelheim Pharmaceuticals, Inc., Merck & Co., Inc., Novo Nordisk Inc. P. Dandona: Advisory Panel; Self; AstraZeneca. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca.