Meal Intake Is Suppressive of Ketogenesis in Patients with Type 1 Diabetes

Aim: To investigate whether the intake of a meal suppresses ketogenesis in patients with type 1 diabetes.

Methods: 30 patients with type 1 diabetes with no C-peptide, fasted overnight, were divided into 3 groups of 10 patients each. The first (group 1) continued the fast for 5 hours after arrival in our clinical research unit while the second (group 2) was administered a high fat high calorie (HFHC) meal without preprandial insulin and the third (group 3) was administered the meal with preprandial insulin. Blood samples were obtained prior to and after the meal at hourly intervals for 5 hours.

Results: In group 1, glucose and glucagon concentrations remained unchanged while FFA concentrations increased (by 74±16%) as did acetoacetate (AcAc) and beta-hydroxybutyrate (BHB) concentrations (by 52±13% and 64±16%, respectively). In group 2, the intake of the meal without preprandial insulin induced marked increase in glucose, glucagon and FFAs (by 235±32%, 81±18% and 75±17%, respectively) concentrations. However, the meal induced significantly lower increase in AcAc or BHB concentrations (increased by 29±9% and 35±11%, respectively) compared to group 1. In group 3, given preprandial insulin before the meal, there was a significant reduction in glucose and glucagon concentrations as compared to group 2 and a fall in FFA concentrations (by 41±12%) below baseline levels. There was no significant increase in AcAc and BHB.

Conclusions: While a prolonged fast was associated with maintenance of glucose and increases in FFA, AcAc and BHB concentrations, the intake of the meal prevented increases in AcAc and BHB in spite of increases in glucose, glucagon and FFA concentrations. These actions are consistent with an anti-ketogenic effect of the meal intake even in type 1 diabetes with an absence of β cell function.