The effect of improved postprandial blood glucose control on postprandial metabolism and markers of vascular risk in people with Type 2 diabetes

Gallagher A. Diabet Res Clin Pract. 2005;67:196-203.

The aim of this study was to determine the effect of a physiological postprandial insulin profile with insulin aspart on the metabolic and haemostatic abnormalities of people with type 2 diabetes. Postprandial hyperglycemia has become an area of interest, since the toxic effect of high glucose concentrations is greatest at this point. Studies have suggested that postprandial hyperglycemia is more predictive than fasting glucose levels of adverse cardiovascular outcome. This study employed a regimen of premeal plus basal insulin to examine the effects of postprandial control on metabolic, haemostatic, and endothelial markers.

The methods of this study consisted of a single center, double-blind, cross over design on 21 insulin-treated type 2 diabetic patients. After converting from twice-daily to premeal plus basal insulin administration, patients were randomized for a 6-week treatment period. Measurements were collected after a test meal at the 6th week of the study. The total daily dosage of premeal insulin aspart was lower than the dosage of human insulin (45±4.5 U/day versus 50±5 U/day, P = .030) Metabolic and biochemical variables such as A1C, cholesterol, triglycerides, apolipoprotein, and blood glucose levels were monitored for statistical significance.

The results of this study suggest that improving postprandial but not overall blood glucose control with insulin aspart does little to improve the basic features of the lipoprotein profile or levels of vascular risk markers. Timed measurements of blood glucose, cholesterol, free insulin, HDL, blood 3-hydroxybutyrate and triglycerides all failed to display significant differences following treatment with human insulin or insulin aspart. Concentrations of lipids and apolipoproteins did not change significantly despite the significant improvement of A1C.

No changes in haemostatic measurements or endothelial dysfunction with improved postprandial blood glucose control were demonstrated. However there were several limitations to this study. Optimal postprandial blood glucose levels were never achieved within the target range of 4.0-6.0 mmol/L preprandially and 5.0-7.5 mmol/L postprandially. The small sample size and short duration further limits the study results. A possible criticism of this study lies within the wide range of baseline glucose concentrations, which could have been eliminated with intravenous insulin infusions overnight prior to the test meal.