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

Effect of Postprandial Glucose Levels on Microvascular Complications

The effects of postprandial hyperglycemia on the development of microvascular complications of diabetes have been well documented. There is evidence that uncontrolled glycemic peaks activate protein kinase C, the enzyme that may link hyperglycemia to microvascular complications.[8] Elevated glucose levels lead to increased intracellular synthesis of diacylglycerol, which, in conjunction with elevated intracellular calcium, activates protein kinase C.[8] The activity of protein kinase C impairs contraction of smooth muscle cells or pericytes, increases production of basement membrane materials, and enhances cell proliferation and capillary permeability. Thus, activation of protein kinase C by postprandial hyperglycemia could be responsible for microvascular complications that may be developing even in the early stages of diabetes.[8]

Data from the National Health and Nutrition Examination Survey showed that patients who had 2-hour postprandial glucose levels of 194 mg/dL had a threefold increase in the incidence of retinopathy, despite normal fasting glucose levels.[3] Studies of Pima Indian and Egyptian populations revealed a similar increase in the incidence of retinopathy in subjects with normal fasting glucose levels but 2-hour postprandial glucose values of >200 mg/dL.[3]

The development of microvascular complications in patients with type 2 diabetes has been documented in a number of clinical trials. In a long-term study of complications in patients who had type 2 diabetes for more than 25 years, Mohan et al[9] reported that postprandial glucose levels were associated with diabetic nephropathy. In a recent study of Pima Indian subjects, hyperfiltration, a precursor of diabetic nephropathy, in subjects with impaired glucose tolerance was found to increase with the onset of type 2 diabetes.[10] In a population study, Beghi et al[11] showed that elevated fasting and postprandial glucose levels, as well as prolonged disease duration, were associated with an increased incidence of diabetic neuropathy.


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