The results of the present study show greater post-supper glucose excursion following an antecedent lunch of high caloric content compared with a lunch of lower content. We could find no reports of similar past studies. Older studies examined the dietary effects on insulin needs using an “artificial pancreas”, termed a Biostator, to regulate glycemia by infusing i.v. insulin based on continuous glucose sensing.7,8
These studies showed that meal macronutrient composition and the time of feeding affect insulin needs. In addition, it is well established that equivalent carbohydrate administration may result in differing meal glucose excursion based on the specific nature (glycemic index) of the food provided.9
Moreover, it is clear that chronic dietary perturbations affect insulin sensitivity.10
However, we could find no study that examined the effect of directly antecedent meal calories on subsequent meal glucose excursion at equivalent pre-meal glycemia.
In the present study, pre-supper glucose, supper food intake, and subcutaneous pre-supper insulin dosing were equivalent after each of the antecedent lunch meals. Moreover, relative nutrient composition at the lunch meal did not differ; the only difference was portion size. Hence, the difference in supper glucose excursion resulted from more calories at lunch. Although post-lunch glycemia was not controlled in the non-diabetic range, these readings do appear representative of those expected in the daily lives of people with Type 1 diabetes.
One limitation of the present study is that our data do not discriminate between the effects of one particular macronutrient type versus another. Another limitation is that there were some asymptomatic low glucose readings in the early portion of the study days for both the high- and low-caloric lunches. However, these all occurred before the lunch meal and required few extra calories, which did not differ according to study day.
There appeared to be a greater immediate pre-supper downward momentum of blood glucose following the larger compared with the smaller lunch (). However, this would not alter data interpretation because the post-supper glycemic excursion following the larger lunch, if anything, would be less if downward glucose momentum carried into the supper meal.
Our intent was to perform this study in a clinically meaningful manner. However, we do acknowledge the limitation that we used i.v. insulin rather than s.c. to maintain post-lunch glycemia. We believe our objective of matching pre-supper glycemia would have been much more difficult if we were dependent on adjustments of s.c. insulin administration, even by CSII. Thus, we examined the effect of differing antecedent food intake with attention to providing enough insulin so that glucose concentrations by the subsequent meal were essentially equivalent. This, in fact, is what patients attempt to achieve on a daily basis by taking meal-time insulin according to carbohydrate and calories consumed.
We considered that higher circulating free fatty acids after the larger lunch may explain the greater glycemic excursion following supper by decreasing muscle glucose utilization.6,11
However, plasma concentrations of free fatty acids did not significantly differ and, if anything, were lower following the larger lunch. This may have resulted from the greater insulin infusion rates required after the larger of the antecedent lunch meals. So, although we can only speculate, it remains possible that even without an increase in pre-supper circulating free fatty acids there could have been an increase in intramyocellular or intrahepatic fat, which would decrease insulin sensitivity at the time of the subsequent meal. In this respect, resistance to insulin is associated with increased triglyceride in the liver and skeletal muscle.12,13
Moreover, postprandial triglyceride accumulation in the liver and skeletal muscle has been documented using 13
C magnetic resonance spectroscopy, at least in subjects with Type 2 diabetes, and postprandial accumulation of liver triglyceride has been documented in non-diabetic subjects.14
In conclusion, caloric intake at an antecedent meal impacts glucose control following a subsequent meal. For optimal postprandial glucose control, patients with Type 1 diabetes may need to consider not only anticipated meal calories, but also prior food intake, a practice not commonly recommended based on currently used insulin algorithms.