Special Article
March 8, 2004

Optimal Glycemic Control in Type 2 Diabetes MellitusFasting and Postprandial Glucose in Context

Author Affiliations

From the Joslin Diabetes Center and Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Mass. Dr Abrahamson has been on the speakers' bureau for the following companies: Aventis, Bristol-Myers Squibb, Eli Lilly, GlaxoSmithKline, Novo Nordisk, Novartis, and Pfizer.


Copyright 2004 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2004

Arch Intern Med. 2004;164(5):486-491. doi:10.1001/archinte.164.5.486

Type 2 diabetes mellitus is the consequence of both insulin resistance and impaired insulin secretion. In the progression from normal glucose tolerance to diabetes, postprandial glucose (PPG) levels often rise before fasting plasma glucose (FPG) levels increase above 126 mg/dL (7.0 mmol/L). Numerous epidemiologic studies have shown that impaired glucose tolerance is associated with increased risk for macrovascular disease and that isolated postchallenge hyperglycemia is an independent factor for increased mortality. Reducing the risk for microvascular complications by improving glycosylated hemoglobin (HbA1c) levels is well documented. Emerging data now support the relationship between glycemic control and macrovascular disease. Epidemiologic studies documenting postprandial hyperglycemia and the risk for increased mortality suggest that lowering PPG levels might be beneficial. Optimizing both FPG and PPG is important in achieving normal/near-normal glucose levels. Many patients with type 2 diabetes have difficulty attaining the recommended HbA1c goal despite normal/near-normal FPG levels; thus, pharmacologic treatment targeting PPG levels may prove beneficial.