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

Methods of Controlling Postprandial Hyperglycemia

Postprandial glycemic control is important in avoiding microvascular and macrovascular complications, lowering insulin resistance, restoring normal insulin secretion, and avoiding complications in the offspring of women with diabetes. It is recommended that the treatment of diabetes include methods that lower both fasting and postprandial glucose levels.

In type I diabetes, postprandial glucose levels can be controlled only with very fast-acting insulin, such as insulin lispro.[36] Lispro differs structurally from regular insulin in the reversal of the two amino acids at positions 28 and 29 on the B chain (proline-lysine to lysine-proline).[36] Subcutaneous regular insulin, especially in large doses, forms a hexamer that has to be broken down to a dimer or a monomer before it can be absorbed into the blood stream to lower plasma glucose. Thus, after a meal, glucose levels rise before subcutaneous regular insulin can be absorbed. In addition, the longer action of regular insulin leads to unphysiologically elevated plasma insulin. Since this state often results in late hypoglycemia, between-meal snacks are needed. Snacking can increase total calorie intake, causing an undesired weight gain. Lispro insulin does not form hexamers, is quickly absorbed into the blood stream, covers the meal appropriately, and does not linger long enough to cause postprandial hypoglycemia or the need for a snack. For similar reasons, a fast-acting lispro-like insulin is needed in patients with type 2 diabetes who take insulin, even if they have some endogenous production, because they lack first-phase insulin release.

New antidiabetic drugs in development, such as the injectable amylin analog pramlintide and glucagon-like insulinotropic polypeptide (GLIP), target the suppression of postprandial hyperglycemia.[37,38] These drugs slow gastric emptying and suppress glucagon production. Pramlintide also replenishes hepatic glycogen stores, and GLIP increases insulin production in response to a meal. Although both agents suppress postprandial hyperglycemia, as yet, neither can be taken orally and therefore must be injected subcutaneously.

In patients with type 2 diabetes who require none or just one evening or nighttime injection of intermediate-acting insulin to control the fasting glucose level, an oral agent capable of stimulating an insulin release sufficient to cover the meal or delay the absorption of glucose from the intestine (bolus agents) should be used. Drugs with these properties should be used in combination with oral agents that lower insulin resistance, decrease hepatic glucose production, or stimulate insulin production (basal agents). This therapy can be described as oral basal-bolus therapy for type 2 diabetes, in contrast to injection-based basal-bolus therapy using insulin for type 1.

Bolus drugs include acarbose, miglitol,[37] repaglinide, and possibly glimepiride. Examples of basal drugs are troglitazone, pioglitazone, rosiglitazone, metformin, long-acting sulfonylureas, and intermediate and long-acting insulins.[39] It is easier to achieve the long-term HbA1c goal ≤7% using basal-bolus therapy, because at this level of control, the biggest contributor to HbA1c values is the postprandial glucose level.[1]

Several drugs that stimulate a short-lived insulin release are in development. Nateglinide, a D-phenylalanine derivative representing a new class of oral antidiabetic agents, stimulates early insulin release in response to elevated glucose levels in the blood by inhibiting the energy-sensitive potassium channels in pancreatic b-cells. This agent enhances, rather than suppresses, insulin release in the presence of high glucose levels. This rapid and short-lived increase in insulin secretion prevents the effects frequently associated with hyperinsulinemia such as postprandial hypoglycemia and weight gain. Nateglinide has a much higher affinity for b-cell potassium channels than for those on smooth muscle cells,[39] which may provide enhanced safety, since potassium channel closure in the myocardium and coronary arteries can result in an increased incidence of cardiac events.[40]

Regardless of the drugs available, for optimal postprandial glycemic control, patients must monitor their glucose levels after eating a meal. When diabetes is poorly controlled, only preprandial glucose readings are necessary. However, once control is achieved, it is important to monitor glucose levels both before and after meals. This allows for appropriate adjustments of bolus drug administration to reach postprandial glycemic goals and to maximize the patient's protection from diabetic complications.

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