Editor
in Chief :
Mahmoud
Ashraf Ibrahim ,MD |
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Issues
per Volume:
Quarterly
Current Volume: 1
Current Issue : 1
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Volume
1 number 1 Summer 2003
Special issue for the abstracts of the 7th Pan Arab Conference
on Diabetes
PACD7 , 25 – 28 March 2003 Cairo
Abstract Number : 36
Postprandial Hyperglycemia—How Important Is It?
Robert Rizza, USA
Individuals with type 2 diabetes are at increased risk of developing micro- and macrovascular complications if their diabetes is not properly treated. Long-term randomized studies have shown that lowering HbA1C concentration result in a continuous and proportionate decrease in the incidence of micro-vascular complications. The goal, therefore, is to keep HbA1C concentrations in people with diabetes as near normal as possible while avoiding hypoglycemia. Since glycosylation of hemoglobin is an index of the integrated exposure of hemoglobin to glucose over a several month period of time, it is presumed that complete normalization of HbA1C requires normalization of both fasting and postprandial glucose concentrations. The word “Postprandial” means, “following a meal.” The magnitude and time of the post-prandial peak in plasma glucose concentration depends on a variety of factors, including the quantity and composition of the meal, the rate of absorption of nutrients, and rate and degree of suppression of endogenous glucose production, and the ability of the liver, muscle and other extrahepatic tissues to take up glucose. Glucose concentrations in nondiabetic humans commonly peak between 45-60 minutes after the start of the meal. The time to peak in diabetic humans varies considerably due in large part to a mismatch between insulin need and insulin availability. Therefore, measurement of glucose concentration at different times following meal ingestion will give it different estimate of the postprandial peak. This perhaps explains the fact that several studies have shown a strong correlation between HbA1C and mean glucose concentration, whereas the correlation between HbA1C and peak postprandial glucose concentrations is weaker.
The cause of postprandial hyperglycemia in individuals who have normal or near normal fasting glucose concentration is an area of active investigation. A variety of studies have shown that an acute rise in glucose and insulin can alter endothelial function and perhaps alter coagulation factors. On the other hand, an acute increase in glucose in the absence of an increase in insulin concentration appears to have minimal, if any, affect on endothelial function, suggesting a primary effect of insulin rather than glucose. However, such studies have been acute, and the effects of chronic versus episodic increases in glucose concentration in diabetic humans is not known. On the other hand, epidemiological data suggest that glucose concentrations observed two hours following glucose ingestion predict the development of cardiovascular disease in nondiabetic humans. Some studies suggest the two-hour glucose concentration is a stronger predictor of cardiovascular disease than is the fasting glucose concentration. In addition, in one study, women with gestational diabetes who were randomly assigned to a group that specifically targeted Postprandial glycemic control had fewer Cesarean sections and a lower incidence of fetal macrosomia than did women who did not specifically target Postprandial glycemic control. It currently is not known whether in the presence of comparable HbA1C concentrations treatments that predominantly lower Postprandial but not fasting hyperglycemia in people with established diabetes result in fewer complications than do treatments that predominantly lower fasting glucose but not Postprandial glucose concentrations. However, it is clear that complete normalization of HbA1C will require restoration of both fasting and postprandial glucose concentrations to those observed in nondiabetic individuals.
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