Type 2 diabetes (T2DM) is a chronic disease characterized by cellular insulin resistance and consequent disturbances in glucose metabolism. Long-term consumption of buckwheat has been previously shown to improve glycemia in individuals with T2DM; however, the underlying mechanisms as well as the contribution of improved acute glycemic responses have not been fully characterized. The current study used cell culture and clinical studies to investigate the mechanisms and effectiveness of common buckwheat for acute modulation of glucose metabolism and glycemia. Glucose uptake was inhibited in H4IIE cells treated with a buckwheat extract (BWE), an effect attributed to the actions of an unknown compound(s). Reduced glucose uptake and transepithelial glucose transport was also present in Caco2 colorectal adenocarcinoma cells and monolayers. The mechanism behind inhibited glucose uptake did not involve modulation of several signaling pathways regulating glucose metabolism, including p38 MAPK, p42/44 ERK, PI3Kγ, PKC, PKA, mTOR and AMPK. Interestingly, BWE treatment was associated with other effects on glucose metabolism, including elevated glucose production and levels of gluconeogenic enzymes. However, these effects were not mediated through the classical pathway of CREB activation involving cyclic AMP and PKA.
In a blinded, reference product-controlled study, consumption of a cracker product made from whole grain common buckwheat flour containing 50 grams of available carbohydrate was not associated with changes in post-prandial glucose or insulin concentrations in both healthy individuals and those with diet-controlled T2DM. However, consumption of buckwheat crackers was associated with changes in selected gastrointestinal satiety hormones. Interestingly, several significant correlations observed between fasting concentrations and the overall post-prandial response of these hormones were affected by T2DM.
In conclusion, glucose-lowering effects of common buckwheat are not due to the actions of known bioactive compounds, and may involve direct inhibition of facilitative transporters by a novel compound. Although a buckwheat food product did not reduce post-prandial glycemia, identifying the compound responsible for inhibited glucose uptake will allow development of food products enriched with this compound, and may represent a more effective dietary approach to managing glycemia.
| Identifer | oai:union.ndltd.org:MANITOBA/oai:mspace.lib.umanitoba.ca:1993/14395 |
| Date | January 2010 |
| Creators | Stringer, Danielle Marie |
| Contributors | Zahradka, Peter (Physiology) Taylor, Carla (Human Nutritional Sciences), Eskin, Michael (Human Nutritional Sciences) Siow, Chris (Physiology) Mathews, Suresh (Auburn University) |
| Publisher | American Chemical Society |
| Source Sets | University of Manitoba Canada |
| Detected Language | English |
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