Prandial Insulin and the Systemic Appearance of Meal-Derived Glucose in People With Type 1 Diabetes

The rate of appearance of meal-derived glucose is determined by a variety of factors. Ingested complex carbohydrates require enzymatic digestion into monosaccharides before absorption. Although this step per se is not rate limiting, the rate of gastric emptying and orocecal transit time may affect the rapidity with which such carbohydrates are exposed to the appropriate digestive enzymes (1). The resulting monosaccharides are then transported into the enterocyte and then into the portal vein where, ultimately, a fraction is extracted by the liver. The remainder is released into systemic circulation via the hepatic venous system. Hepatic extraction of meal-derived glucose is largely dependent on the prevailing glucose and, to a lesser extent, insulin concentrations.

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. This is a finding that at face value might have profound implications for affected patients treated with intensive insulin therapy.

There is limited information on splanchnic extraction in type 1 diabetes. Nuclear magnetic resonance spectroscopy has demonstrated that in people with poorly controlled type 1 diabetes, glycogen synthesis is markedly impaired after ingestion of a mixed meal (3). On the other hand, a similar series of experiments under hyperinsulinemic-euglycemic conditions concluded that there was no difference in hepatic glycogen synthesis between people with well-controlled type 1 diabetes and healthy control subjects (4).

The applicability of these experiments to the splanchnic extraction of enterally delivered glucose is uncertain. However, in a …