Review
Postprandial Hyperglycemia/Hyperlipidemia (Postprandial Dysmetabolism) Is a Cardiovascular Risk Factor

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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.

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Cardiovascular Risk of Postprandial Hyperglycemia

Recent studies have indicated that almost 2 of 3 patients who present with symptomatic CHD have abnormal glucose homeostasis.4 A significant proportion of these at-risk subjects would go undetected when screened with fasting glucose levels but would demonstrate hyperglycemia after meals or during oral glucose tolerance tests.5 Glucose tolerance is generally established by administering a 75-g glucose load in the fasting state. Impaired glucose tolerance, or prediabetes, is defined as a 2-hour

Postprandial Hyperlipidemia

Postprandial hyperlipidemia with elevated levels of triglycerides, chylomicron remnants, and free fatty acids results in oxidative stress and inflammation and may independently potentiate the adverse effects of postprandial hyperglycemia.1, 15 These elevated and protracted postmeal lipid levels are features of insulin resistance.

Triglycerides are traditionally measured in the fasting state, typically the lowest triglyceride level of the day. Levels of fasting and postprandial triglycerides are

How Postprandial Dysmetabolism Induces Atherosclerosis

Excessive intake of high-calorie, quickly digestible food results in abnormal surges in blood glucose, triglyceride, and free fatty acid levels. This bolus of energetic substrates essentially swamps the metabolic capabilities of the mitochondria in the overnourished muscle and adipose tissues.19 Glucose and free fatty acids overwhelm the Krebs cycle, stimulating excess production of nicotinamide adenine dinucleotide that outpaces the capacity for oxidative phosphorylation. This buildup of

Diet and exercise

Altering the type and/or amount of dietary carbohydrates can improve postprandial glucose and HbA1c levels.25, 26 The glycemic index is determined by comparing the increase in blood glucose after 50 g of a specific food with that noted after 50 g of oral glucose. Most prospective observational studies show that diets rich in high-glycemic index foods, especially when combined with low dietary fiber content, are independently associated with the development of type 2 diabetes and CHD.25

The

Pharmacologic Therapy for Postprandial Dysmetabolism

Statins exert strong intracellular antioxidant activity,1, 19 and these agents have been to shown to reduce inflammation and protect endothelial function in nondiabetic and diabetic subjects. Long-term statin therapy can reduce postprandial remnant lipoproteins.37 A recent study showed that atorvastatin acutely reduced the adverse effects of postprandial dysmetabolism in diabetic subjects.1 Short-term therapy with atorvastatin has been shown to blunt the postprandial increases in oxidative

Acknowledgment

We would like to acknowledge Jose Aceituno, who created the figures for this report, and Lori J. Wilson, who assisted with manuscript preparation.

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