Submitted to: Pediatric Diabetes
Publication Type: Peer reviewed journal
Publication Acceptance Date: 5/19/2008
Publication Date: 12/9/2008
Citation: Heptulla, R.A., Rodriguez, L.M., Mason, K.J., Haymond, M.W. 2008. Gastric emptying and postprandial glucose excursions in adolescents with type 1 diabetes. Pediatric Diabetes. 9(6):561-566. Interpretive Summary: Amylin is a hormone produced in the pancreas. Amylin and insulin are released at the same time from the pancreas. Both amylin and insulin are low in people with type 1 diabetes. Amylin works by slowing the release of food from the stomach and lowering glucagon levels after the meal. We were interested in whether children with type 1 diabetes make amylin and if they had faster food release from the stomach. To study this we gave a mixed meal, and we measured amylin, glucagon, insulin, glucose, and the rate of food release from the stomach. We studied seven children with type 1 diabetes and eight healthy children without diabetes. We compared the two groups to identify differences. From this study we found that children with type 1 diabetes had very high blood sugar levels when compared to the healthy children. As we anticipated, amylin levels were low in the children with type 1 diabetes when we compared them to healthy children. The insulin levels in children with type 1 did not go up after they ate their meal. The glucagon levels were not different between the two groups. It was very interesting to find that children with type 1 diabetes had a much slower release of the meal from the stomach when compared to the healthy children. From this study we concluded that children with type 1 diabetes have low amylin levels and the release of the food from the stomach was slow and not fast. We think there are other things, in addition to amylin, controlling the rate of food release from the stomach in type 1 diabetes. Also we learned from our study, that insulin shots are not very effective in increasing the levels of insulin in the blood and helping to lower the post meal sugar.
Technical Abstract: Because amylin is co-secreted with insulin from beta cells, patients with type 1 diabetes (T1DM) are deficient in both insulin and amylin. Amylin delays gastric emptying and suppresses glucagon in the postprandial period. Hence, we hypothesized that children with complication-naive T1DM have accelerated gastric emptying in response to a mixed meal because of amylin deficiency. Amylin, glucagon, insulin, glucose, and gastric emptying were measured in seven T1DM and in eight control subjects without diabetes. Subjects with T1DM had markedly elevated glucose concentrations when compared with controls (p < 0.0001). Amylin concentrations as predicted were lower in T1DM compared with those in controls (p < 0.0001). Insulin did not peak in the immediate postprandial period in T1DM when compared with controls (p < 0.0001). Glucagon concentrations did not significantly differ between groups. Interestingly, gastric velocity was delayed in patients with T1DM compared with controls (p < 0.01). In conclusion, subjects with T1DM do have amylin deficiency but this is not associated with accelerated gastric emptying as we had hypothesized but rather with delayed gastric emptying. Factors other than amylin play a role in control of gastric motility in T1DM. Subcutaneous insulin delivery fails to reach adequate concentrations in the postprandial period to curtail peak glucose concentration in T1DM.