The effect of glycaemic control on fibrin network structure of type 2 diabetic subjects

• Published in: Thrombosis and haemostasis Vol. 96; no. 5; p. 623
• Main Authors: Pieters, Marlien, Covic, Namukolo, Loots, Du Toit, van der Westhuizen, Francois H, van Zyl, Danie G, Rheeder, Paul, Jerling, Johann C, Weisel, John W
• Format: Journal Article
• Language: English
• Published: Germany 01-11-2006
• Subjects: Adult; Aged; Blood Coagulation; Blood Glucose - analysis; Blood Glucose - physiology; Diabetes Mellitus, Type 2 - blood; Female; Fibrin - chemistry; Fibrin - ultrastructure; Fibrinogen - analogs & derivatives; Fibrinogen - analysis; Fibrinogen - metabolism; Glycosylation; Humans; Insulin - administration & dosage; Insulin - pharmacology; Male; Middle Aged; Porosity
• ISSN: 0340-6245
• DOI: 10.1160/TH06-07-0390

Diabetic subjects have been shown to have altered fibrin network structures. One possible cause may be fibrinogen glycation resulting in altered structure/function properties. We investigated the effect of glucose control on fibrinogen glycation and fibrin network structure in type 2 diabetes. Blood samples were taken from twenty uncontrolled diabetic subjects at baseline to determine the levels of fibrinogen glycation and fibrin network structures. The subjects were then treated with insulin until blood glucose control was achieved before end blood samples were taken. Twenty age- and BMI-matched non-diabetic subjects were included as a reference group. The diabetic subjects had significantly higher mean fibrinogen glycation at baseline than the non-diabetic subjects (7.84 vs. 3.89 mol glucose / mol fibrinogen; p < 0.001). This was significantly reduced during the intervention (7.84 to 5.24 mol glucose / mol fibrinogen; p < 0.0002) in the diabetic group. Both groups had high mean fibrinogen concentrations (4.25 and 4.02 g/l, diabetic and non-diabetic subjects respectively). There was no difference in fibrinogen concentration, porosity, compaction and kinetics of clot formation between the diabetic subjects and non-diabetic subjects at baseline, nor were there any changes during the intervention despite the reduced fibrinogen glycation. Fibrin network characteristics correlated well with fibrinogen but not with any markers of glycaemic control. Improved glycaemic control resulted in decreased fibrinogen glycation but not fibrinogen concentration. It seems as though porosity, compaction and kinetics of clot formation are more related to fibrinogen concentration than fibrinogen glycation in this model.