Post-prandial hyperglycemia (PPH) is mainly attributed to a reduced first phase insulin secretion and lesser to insulin resistance. Although a marker of post-prandial glycemia (PPG), 2-hour post glucose load glycemic level (2hG) has low reproducibility. PPH is an important cardiovascular (CV) risk factor, particularly in DM in which CV diseases are the main cause of death. In non-diabetics, fasting and/or 2hG increase such risk, which occurs in a continuum within the normal range (dysglycemia). Atherosclerotic lesions are more pronounced in glucose metabolism disturbances; an association of arterial injury and 2hG was verified. In populations with normal fasting glycemia the risk of death increases along with 2hG. Non-enzymatic glycation of arterial wall components and lipoprotein oxidation accelerate atherosclerotic process. PPH is associated with conduction disturbances, which facilitate the occurrence of sudden death. Endothelial dysfunction could also predispose to vasoconstriction and post-prandial myocardial ischemia. ADA recommends that PPG should be monitored, especially when fasting glycemia and A1c are not proportional. While the efficacy of alpha-glucosidase inhibitors, glynides and ultra-short action insulin analogues are proved to reduce PPG it is still necessary to ascertain whether they are able to reduce long-term diabetic complications.
Post-prandial hyperglycemia; Cardiovascular risk; Mortality; Glucose intolerance