A Break in the Brake Mechanism in Diabetes

A cause of postprandial hyperglycemia

The importance of insulin and glucagon as fine regulators of glycemic excursions is well established (1). Alterations in gastric emptying are generally not considered important contributors to postprandial hyperglycemia until late complications of diabetes such as gastroparesis have occurred (2,3). It is now emerging that the rate of gastric emptying may be a major determinant of postprandial glycemic excursions in healthy subjects, as well as in type 1 and type 2 diabetic patients (4).

Gastroparesis is a relatively rare complication that occurs late in diabetes because of irreversible intestinal nerve damage (4); it must be distinguished from the physiological inhibitory effects of acute hyperglycemia on gastric motility (5,6). The latter has been proposed as a defense mechanism existing to minimize postprandial hyperglycemia by reducing the rate of efflux of glucose into the circulation from the gut (7). This may be of special importance for people with type 1 diabetes who have a reduced ability to delay gastric emptying in response to hyperglycemia (8). Cross-sectional studies suggest that an inverse relationship between the rate of gastric emptying and blood glucose concentration also exists in type 2 diabetic patients (4) and, thus, that similar regulatory mechanisms may exist in both conditions.