Postprandial hyperglycemia in patients with type 2 diabetes mellitus

Abstract

The role of postprandial hyperglycemia (PPHG) in diabetes mellitus is being increasingly recognized. It is known that PPHG contributes to the increased risk of both micro- and macrovascular complications in patients with diabetes mellitus. This review looks at the clinical significance of PPHG and the currently available therapeutic modalities. The causes of PPHG are influenced by many factors which include a rapid flux of glucose from the gut, impaired insulin release, endogenous glucose production by the liver and peripheral insulin resistance. Knowledge of the pathophysiology of PPHG is essential when adopting treatment options to tackle the problem. Although most oral antihyperglycemic agents and insulins lower both fasting and postprandial blood glucose levels, drugs are now available which specifically act to control PPHG. These drugs may be classified based on the site of their action. a-Glucosidase inhibitors like acarbose and miglitol attenuate the rate of absorption of sucrose by acting on the luminal enzymes. Adverse effects of these agents are predominantly gastrointestinal. Newer insulin secretagogues have been developed which attempt to mimic the physiological release of insulin and thus ameliorate PPHG. These include third generation sulfonylureas like glimepiride and nonsulfonylurea secretagogues like repaglinide and nateglinide. Rapid-acting insulin analogs, the amino acid sequences of which have been altered such that they have a faster onset of action, help to specifically target PPHG. Pre-mixed formulations of the analogs have also been developed. Finally, drugs under development which hold promise in the management of patients with PPHG include pramlintide, an amylin analog, and glucagon-like peptide-1 and its analogs.