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Exact(4)

We used a standardized triple-tracer mixed meal to enable measurement of the rate of meal appearance, endogenous glucose production, and glucose disappearance.

41 However, the rate of meal appearance as assessed by a radiolabeled standard meal was lowered, suggesting that perhaps splanchnic sequestration of meal-derived glucose may play a role in lowering glucose concentrations.

Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of endogenous glucose production (EGP) was slightly delayed and the increment in glucose disappearance was substantially lower (P < 0.01) in diabetic subjects during the first 3 h after meal ingestion.

Model components describing the effects of insulin and glucose at zero insulin to increase glucose uptake and decrease endogenous glucose production are derived from the minimal model equations of Bergman et al. and the model describing the rate of meal glucose appearance follows from work by Wilinska et al. The combined model (Appendix, Eqs.

Similar(56)

Intriguingly, in this issue of Diabetes Care, Pennant et al. (2) report that the rate of meal-derived glucose appearance in people with type 1 diabetes is unchanged by administration of prandial insulin 20 min before meal ingestion.

In the Japanese studies, a higher elimination rate of meal-related symptoms was also seen with acotiamide, and 100 mg three times a day was established as the optimal dose.

22 The systemic rates of meal appearance (Rameal), EGP, and glucose disappearance were calculated using Steele's two compartment model.

These studies are in agreement with the current work, where insulin and glucose levels did not appear to affect rates of meal glucose appearance.

Despite insulin deficiency and fasting and postprandial hyperglycemia, people with untreated diabetes showed no difference in Rameal compared with healthy individuals (7), and following intensive insulin therapy, there was similarly no difference in rates of meal glucose appearance.

This impairment contributes to exaggerated rates of meal-derived glucose appearance and, ultimately, postprandial glucose excursions.

Moreover, our studies demonstrate that this impairment leads to exaggerated rates of meal-derived glucose appearance in plasma and thus contributes to postprandial hyperglycemia.

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