Prandial glucose regulation in the glucose triad - Emerging evidence and insights

While it is well established that overall glycemic control reduces the complications of diabetes, the role of fasting glycemia versus postprandial glycemia in the pathophysiology of diabetes and its complications, and the relative importance of these parameters as specific targets of therapy, remain controversial. Evidence that postprandial glucose (PPG) plays an independent, modifiable role in cardiovascular disease is accumulating, largely from epidemiological studies. A large number of epidemiological studies show that high postprandial glucose is an independent risk factor for cardiovascular disease: indeed, a more powerful risk factor than fasting glucose or HbA(1c). Pathophysiological hypotheses that support these observations include the contribution of postprandial glucose to HbA(1c); postprandial glucose as a surrogate marker for other cardiovascular risk factors, serum lipids and triglycerides in particular; and direct toxicity of elevated glucose levels attributed to "spikes" in glucose concentration following caloric ingestion. Early interventional data suggest that therapy targeted at postprandial glucose can have a favorable impact on cardiovascular events. While more interventional studies clearly are needed, the growing weight of evidence supports a therapeutic approach more directed at excessive prandial glycemic excursions that are characteristic of both type 1 and type 2 diabetes.