Importance of Postprandial Glucose Control

, Department of Medicine, University of Alabama at Birmingham School of Medicine

South Med J. 2001;94(8) 

In This Article

Postprandial Glucose Levels and Macrovascular Complications

The glycemic threshold for the development of macrovascular complications is lower than that for microvascular complications, so there is more evidence for an association with postprandial glycemia. Postprandial glucose elevations are associated with postprandial hyperinsulinemia and higher plasma levels of triglycerides, chylomicrons, chylomicron remnants, and free fatty acids. High concentrations of free fatty acids have been associated with endothelial dysfunction,[12] and high triglyceride levels have been linked to low levels of high-density lipoprotein (HDL) cholesterol and a preponderance of small, dense, low-density lipoprotein (LDL) particles. Although only the relationship between fasting-state hypertriglyceridemia and coronary artery disease (CAD) has been established, postprandial high triglyceride levels most likely have the same effect.[13] In addition, high postprandial glucose levels result in protein and cellular glycosylation. Glycosylated LDL particles are more easily oxidized and taken up by macrophages through the scavenger receptor. This, in turn, leads to higher foam cell production, and, ultimately, atherosclerotic plaque. In addition, glycosylated LDL also stimulates platelet aggregation. Glycosylated HDL is less efficient than nonglycosylated in transporting cholesterol back to the liver for metabolism. Additionally, the formation of advanced glycosylated end products in the collagen of the vessel wall itself may directly stimulate or accelerate the atherosclerotic process.[14]

Acute increases in plasma glucose also stimulate the production of free radicals, another factor involved in the atherosclerotic process.[15] Excessive postprandial plasma glucose levels have also been associated with transient hypercoagulability resulting from increased thrombin production and decreased fibrinogen breakdown. These, in turn, result from the overproduction of plasminogen activator inhibitor, which directly inhibits tissue plasminogen activator activity. Control of postprandial hyperglycemia reverses this hypercoagulable state.[16]

Endothelial dysfunction is another consequence of postprandial hyperglycemia. Activation of protein kinase C in the endothelium increases adhesion molecules[17] that facilitate leukocyte uptake into the blood vessel wall; increases production of the vasodilators nitric oxide and prostaglandin; increases expression of the vasoconstrictor endothelin; and induces platelet aggregation.[8]

The Honolulu Heart Study found that the risk of CAD correlated with plasma glucose levels measured 1 hour after a 50-g oral glucose load. The incidence of CAD was twice as high in patients with postprandial plasma glucose levels between 157 and 189 mg/dL as in those with levels <144 mg/dL,[18] and the incidence of sudden death was doubled with postprandial plasma glucose levels >151 mg/dL.[19] The Whitehall Study of British male civil servants showed that plasma glucose levels >96 mg/dL 2 hours after a meal were associated with a twofold increase in mortality from CAD.[20] Another British study, the Islington Diabetes Survey, reported that the incidence of major CAD (defined as major electrocardiographic changes or myocardial infarction) was 17% in subjects with a 2-hour postprandial glucose level between 120 and 180 mg/dL, compared with 9% in subjects with levels <120 mg/dL.[21] The Bedford Survey showed that protection from CAD was lost in patients with elevated postprandial glucose.[22] By studying the progression of CAD in young men with previous myocardial infarction, Bavenholm et al[23] found that fasting and postprandial plasma glucose levels were independently related to disease progression. The Oslo Study indicated that the nonfasting plasma glucose level was a predictor of fatal stroke in diabetic patients, with the risk increasing by 13% for each 18-mg/dL elevation in postprandial glucose.[24] The Diabetes Intervention Study also showed that postprandial, not fasting, hyperglycemia was an independent risk factor for myocardial infarction and cardiac death.[25]

The Hoorn Study documented an increased risk of peripheral vascular disease in elderly patients with diabetes and in subjects with impaired glucose tolerance.[26] Ankle to brachial pressure indices <0.9 were found in 7% of nondiabetic subjects, 9.5% of subjects with impaired glucose tolerance, 15.1% of patients with newly diagnosed diabetes, and 20.9% of patients with established type 2 diabetes. After logistical regression analysis and correction for other cardiovascular risk factors, the 2-hour postprandial plasma glucose value remained an independent risk factor for peripheral vascular disease, whereas plasma insulin did not.[26]

Overexposure to insulin in response to postprandial hyperglycemia has been shown to be a risk factor for cardiovascular events. The Paris Prospective Study found that postprandial hyperinsulinemia was a better predictor for fatal CAD than either hyperglycemia or diabetes.[27] Similarly, the Helsinki Policemen Study revealed an independent association between fatal and nonfatal CAD events and 1- and 2-hour postprandial insulin levels that was stronger than that with fasting plasma insulin levels.[28] Finally, a recent report suggested an association between postprandial levels and intellectual function in elderly Alzheimer's patients who were not ApoE4 positive.[29]

Another factor associated with postprandial hyperglycemia is postprandial hyperlipidemia. Elevated triglyceride levels after a meal predict the development of CAD and are associated with carotid artery atherosclerosis in nonobese white subjects.[30] Therefore, a reduction of postprandial glucose levels, which also reduces plasma insulin and lipids after a meal, could reduce the incidence of CAD.

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