How should postprandial glycemia be treated?

Abstract

In an attempt to prevent the complications of type 2 diabetes, particular attention should be paid to controlling postprandial glycemia (PPG): on the one hand, it contributes substantially to the HbAlc level in moderately controlled patients, on the other hand, the postprandial glucose peak induces oxidative stress and endothelial dysfunction, the first step toward accelerated atherogenesis. Metformin, glitazones, and insulin secretagogues have an additive effect on fasting blood glucose (FBG), and a significant impact on PPG. Alpha-glucosidase inhibitors can reduce PPG by a mean 0.50 g/l, no matter what the insulin resistance or insulinopenia status or the other diabetes treatments already in use. After evolving for several years and the failure of oral antidiabetics to normalize fasting blood glucose, long-acting (slow-acting) insulin analogues, well titrated, can reach this goal. They will have no effect on PPG other than a simple level effect. At this stage, rather than overtreating high fasting blood glucose concentrations, systematic PPG exploration should be the rule so as to better define PPG treatment: the advantages of alpha-glucosidase inhibitors and the role of GLP-1 analogs should be defined, the use of a rapid-acting insulin analog before the meal causing the highest postprandial blood glucose excursions, even systematically at all three meals, should be considered, or inhaled insulin. As natural life expectancy is on the rise, these active strategies designed to normalize the daily glycemic profile, necessary in a strict strategy to prevent the complications of diabetes, will need to be discussed for an increasing number of patients with type 2 diabetes.