Islet dysfunction and peripheral
insulin resistance are both present in
type 2 diabetes and are both necessary for the development of
hyperglycemia. In both type 1 and
type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as
glycated hemoglobin (HbA1c), and vascular
diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be <7%. The measurement of the HbA1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of
blood glucose excursions, but provides an overall mean value only.
Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal
glucose excursions is as important as controlling fasting plasma
glucose in persons with diabetes and
impaired glucose tolerance. Evidence exists for a causal relation between postmeal
glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial
glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in
diabetic complications, including oxidative stress, endothelial dysfunction,
inflammation, and
nuclear factor-kappaB activation. The goal of
therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of
glycemic control: HbA1c, fasting
glucose, and postmeal
glucose peak.