Postprandial hyperglycemia/hyperlipidemia (postprandial dysmetabolism) is a cardiovascular risk factor.
Epidemiologic data indicate that a postprandial state characterized by abnormally increased levels of glucose and lipids (also referred to as postprandial dysmetabolism) is an independent predictor of future cardiovascular events, even in nondiabetic subjects. The cardiovascular toxicity of postprandial dysmetabolism is mediated by oxidant stress, which is directly proportional to the increase in glucose after a meal. This transient increase in free radicals acutely triggers inflammation, endothelial dysfunction, hypercoagulability, sympathetic hyperactivity, and a cascade of other atherogenic changes. The postprandial dysmetabolism hypothesis has been bolstered by interventional studies that have demonstrated that blunting the postprandial spikes in glucose and lipids improves inflammation and endothelial function immediately. Early randomized controlled trials indicate that reducing postprandial dysmetabolism appears to significantly slow atherosclerotic progression and may improve cardiovascular prognosis. In conclusion, postprandial dysmetabolism appears to be an important proximate cause of adverse cardiovascular events. Addressing this fundamental and largely unrecognized condition will require specific screening and treatment strategies. Diet, exercise, and various pharmacologic agents can improve postprandial dysmetabolism. Using these strategies may help improve the prognosis for patients with diabetes mellitus and/or coronary heart disease.
O'Keefe
James H
JH
University of Missouri-Kansas City, Kansas City, Missouri, USA. jhokeefe@cc-pc.com
Bell
David S H
DS
D050197:Atherosclerosis / Q000209:etiology*; D001786:Blood Glucose / Q000032:analysis; D003327:Coronary Disease / Q000209:etiology*; D004032:Diet; D015444:Exercise; D005609:Free Radicals / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000150:complications*; D006949:Hyperlipidemias / Q000150:complications*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology; D019518:Postprandial Period / Q000502:physiology*; D011379:Prognosis; D012307:Risk Factors
D001786:Blood Glucose; D005609:Free Radicals; D007004:Hypoglycemic Agents; D000960:Hypolipidemic Agents; D008055:Lipids