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

First-Phase Insulin Release

One of the earliest changes in the development of type 2 diabetes is the loss of first-phase insulin release, which occurs with fasting glucose levels of about 110 mg/dL. The loss can be documented by measuring plasma insulin concentrations over the 10 minutes immediately after an intravenous glucose load, calculated on the basis of the patient's weight. Lack of first-phase insulin release, an excellent predictor of both types of diabetes, is thought to be the earliest sign of the adverse effects of hyperglycemia on insulin-producing b-cells and insulin-sensitive tissues (glucotoxicity).[4] When the first-phase insulin response fails, plasma glucose levels rise sharply after a meal. Initially, this precipitates an increased stimulation of second-phase insulin release that, in the early stages of glucose intolerance, may lead to postprandial hypoglycemia resulting from elevated plasma insulin remaining after the nutrients have disappeared.[5] High insulin levels also cause downregulation of the insulin postreceptor pathways on the muscle and fat cells, thus increasing insulin resistance.[6]

The higher glucose level in islet cells prompts a decrease in glucose-transporter activity, resulting in a reduction of insulin release,[7] which is reversed by a decrease in plasma glucose level. If there is no decrease, the prolonged hyperglyce-mia will eventually cause an accelerated loss of insulin-producing b-cells in both type 1 and type 2 diabetes.[4] Thus, metabolic loss of first-phase insulin release results in postprandial hyperglycemia, an increase in insulin resistance, and a further decrease in insulin production.

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