Gastric emptying impairment contributed to meal-derived glucose appearance

Delaying gastric emptying in response to hyperglycemia was impaired in patients with type 1 diabetes and contributed to exaggerated rates of meal-derived glucose appearance and postprandial glucose excursions.

The researchers examined consequences of euglycemia- and hyperglycemia-induced changes in gastric emptying on postprandial glucose fluxes and excursions. They enrolled 15 participants with type 1 diabetes and 10 without diabetes.

Gastric emptying was more common in patients with diabetes (90 minutes to 120 minutes; P<.03). Hyperglycemia delayed gastric emptying in patients without diabetes (222 minutes vs. 167 minutes; P=.003), but did not change in patients with diabetes (148 minutes vs. 152 minutes; P=.51).

Researchers found that plasma islet amyloid polypeptide was undetectable in those with diabetes and replacement slowed gastric emptying to a comparable extent. Meal-derived glucose appearance in plasma decreased 6.8 mcmol x kg^–1 x minute^–1 (P<.001) and splanchnic glucose sequestration increased 25% (P=.04), according to the study. – by Christen Haigh

Diabetes Care. 2008;31:2325-2331.

The results of this study provide some valuable insight into the peculiar problem of excessive postprandial glycemic excursions in patients with type 1 diabetes. It would be desirable, in the presence of hyperglycemia, for gastric emptying to be slightly delayed in the presence of premeal hyperglycemia so that corrective rapid-acting insulin added to the usual mealtime bolus both corrects the hyperglycemia and prevents postprandial hypoglycemia. Knowing that this does not happen in many of our patients with type 1 diabetes provides one more incentive to use rapid-acting analogs with quick onset of action to catch a peak postprandial glycemic excursion that is likely to be very excessive.

– Stephen A. Brietzke, MD
Endocrine Today Editorial Board member