Clinical Significance of Targeting Postprandial Hyperglycemia

Pathophysiology of Type 2 Diabetes

In healthy individuals, normal insulin secretion in response to intravenous glucose follows a biphasic pattern.[2] A rapid, sharp release of insulin into the portal circulation starts within minutes of glucose administration, lasts for about 10 min, and is followed by a slower and more prolonged phase of insulin release that begins at 10 min and lasts between 60 and 120 min.[2] Critical to the regulation of prandial and postprandial glycemia, the first phase of insulin secretion inhibits hepatic glucose production early in the absorptive state, whereas the second phase of secretion attenuates postprandial excursions by promoting glucose uptake by peripheral tissues.[2] Figure 1 illustrates the normal insulin response to an intravenous glucose tolerance test.[2] In individuals with type 2 diabetes, who have insulin resistance, the insulin secretory response can initially compensate for the insulin resistance; however, eventually, first-phase insulin secretion is lost, and second-phase secretion is impaired, causing postpran-dial hyperglycemia, one of the earliest markers of disease progression.[3] Abnormalities in hepatic, pancreatic and muscle metabolism all result from longstanding hyperglycemia.[4] By the time most patients experience symptoms significant enough to cause them to seek medical attention, type 2 diabetes has often been present, unrecognized, for years.

Figure 1. (click image to zoom) The normal two-phase response of insulin to an intravenously administered glucose bolus. Adapted with permission from Pfeifer et al.[2]

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