Pathophysiologic mechanisms of postprandial hyperglycemia

Abstract The role of postprandial hyperglycemia in the etiology of diabetes-related complications and outcomes, although still being elucidated, is greater than previously thought. Acute glucose elevations after meal ingestion are associated with a variety of glucose-mediated tissue defects—oxidative stress, glycation, and advanced glycation end product formation—which have far-reaching structural and functional consequences for virtually every human organ system. Lowering glycosylated hemoglobin to levels that prevent or delay these complications can be achieved only by reducing both postprandial and fasting plasma glucose levels. The α-glucosidase inhibitors (acarbose, voglibose, miglitol) have been effective in delaying the digestion and absorption of carbohydrates, thus diminishing the postprandial surge in blood glucose levels without loss of calories. However, greater emphasis needs to be placed on the measurement of postprandial glycemia, so that readings can be used to guide treatment.