Meal-induced platelet activation in diabetes mellitus type 1 or type 2 is related to postprandial insulin rather than glucose levels. Issue 141 (May 2016)

• Record Type: Journal Article
• Authors: Spectre, Galia; Stålesen, Ragnhild; Östenson, Claes-Göran; Hjemdahl, Paul
• Is Part Of: Thrombosis research. Issue 141(2016)
• Page Start: 93
• Page End: 97
• Publication Date: 2016-05
• Subjects: Platelet activation -- Postprandial -- Insulin -- Glucose; Thrombosis -- Periodicals; 616.135
• DOI: 10.1016/j.thromres.2016.03.009
• Languages: English
• ISSNs: 0049-3848

Abstract

Abstract: Aim: Postprandial platelet activation was related to postprandial insulin rather than glucose levels in a previous meal insulin study in type 2 diabetes mellitus (T2DM). We therefore compared postprandial platelet activation in type 1 (T1DM) patients without insulin secretion and T2DM patients with high postprandial insulin levels. Material and methods: Patients with T1DM ( n = 11) and T2DM ( n = 12) were studied before and 90 min after a standardized meal without premeal insulin. Five T1DM patients volunteered for a restudy with their regular premeal insulin. Platelet activation was assessed by flow cytometry, with and without the thromboxane analogue U46619 or ADP, and by whole blood aggregometry (Multiplate®). Effects of insulin (100 μU/mL) in vitro were also studied. Results: Before the meal, glucose, insulin and platelet activation markers other than platelet-leukocyte aggregates (PLAs) were similar in T1DM and T2DM; PLAs were higher in T1DM. Postprandial glucose levels increased more markedly in T1DM (to 22.1 ± 1.4 vs. 11.2 ± 0.6 mmol/L) while insulin levels increased only in T2DM (from 24.4 ± 4.4 to 68.8 ± 12.3 μU/mL). Platelet P-selectin expression, fibrinogen binding and PLA formation stimulated by U46619 were markedly enhanced (approximately doubled) and whole blood aggregation stimulated by U46619 was increased (p < 0.05 for all) after the meal in T2DM patients but not in T1DM patients. The pilot study with premeal insulin in T1DM patients showed postprandial platelet activation when postprandial insulin levels increased. In vitro insulin mildly activated platelets in both groups. Conclusion: Postprandial platelet activation via the thromboxane pathway is related to postprandial hyperinsulinemia and not to postprandial hyperglycaemia in patients with diabetes. Highlights: Patients with T1DM do not respond with postprandial platelet activation despite very high postprandial glucose levels when premeal insulin is not given. Platelet activation occurred in patients with T1DM after premeal insulin similarly as in patients with T2DM with or without premeal insulin. Our findings support the hypothesis that insulin rather than glucose is responsible for postprandial platelet activation. These findings are of interest as some reports suggest that insulin treatment may worsen cardiovascular outcomes among patients with diabetes.