Postprandial Glycemia: An Important Consideration in Atherosclerosis

Robert S. Rosenson, M.D.
Preventive Cardiology Center
Northwestern University, Feinberg School of Medicine
201 East Huron Street
Galter Pavilion, Suite 11-120
Chicago, IL 60611
Telephone: 312-695-0013; Fax: 312-695-0047; email: r-rosenson@northwestern.edu

Cardiovascular disease is the leading cause of morbidity and mortality among type 2 diabetes patients, however in the National Health and Nutrition Examination Survey III this heightened risk was predominately observed in diabetes patients with manifestations of the metabolic syndrome1 as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III).2 According to ATP III abnormal glucose (? 110 mg/dL) is simply one of five criteria of the metabolic syndrome, and thus dissimilar from the requisite inclusion of insulin resistance by the World Health Organization.3 In epidemiological studies, postprandial hyperglycemia is a more powerful cardiovascular risk factor than fasting hyperglycemia.4

The Campanian Postprandial Hyperglycemic Study5 investigated the relation of postprandial hyperglycemia with carotid intimal medical thickness and inflammatory markers in type 2 diabetes patients, and compared the effects of two insulin secretagogue glyburide (5 to 20 mg/d) and repaglinide (1.5 to 12 mg/d) on carotid intimate medical thickness. Glyburide is a long-acting sulfonylurea and repaglinide is a rapidly acting, short duration insulinotropic agent. The study included 175 drug-naive type 2 diabetes patients aged 35 to 57 years with a body mass index (BMI) ? 24 kg/m2 and 401 control subjects. Carotid intimal medial thickness correlated with glucose peak, IL-6, and hs-CRP in a multivariate model that included age, gender, BMI, fasting glucose and peak postprandial glucose, HbA1c, blood pressure, lipids, IL-6, IL-18, IL-10, and hs-CRP.

After a 12-month intervention there was a similar decrease in HbA1c of 0.9% in both treatment groups; however post prandial glucose levels fell more (p < 0.01) among repaglinide-treated patients (148 ? 28 mg/dL) than glyburide-treated patients (180 ? 32 mg/dL). Carotid intimal medial thickness regression (defined by as a decrease > 0.20 mm) was seen in 52% of diabetes patients assigned to repaglinide and in 18% of patients assigned to glyburide (p < 0.01). Further IL-6 (p = 0.04) and hs-CRP (p = 0.02) fell more in repaglinide-treated patients than glyburide-treated patients. In a multivariate model, changes in carotid intimal medial thickness were explained by changes in glucose peak (28%, p = 0.002), HbA1c (15%, p = 0.013), and hs-CRP, p = 0.01) levels.

This study demonstrated that improvement in peak postprandial glucose was more effective in reducing carotid intimal medial thickness than lowering fasting hyperglycemia. Future cardiovascular disease prevention studies in type 2 diabetes patients should consider fasting and postprandial glucose levels.

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