Thromb Haemost 2006; 96(05): 623-629
DOI: 10.1160/TH06-07-0390
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

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

Marlien Pieters
1   Department of Nutrition, North-West University, Potchefstroom, South Africa
,
Namukolo Covic
1   Department of Nutrition, North-West University, Potchefstroom, South Africa
,
Du Toit Loots
1   Department of Nutrition, North-West University, Potchefstroom, South Africa
,
Francois H. van der Westhuizen
2   School of Biochemistry, North-West University, Potchefstroom, South Africa
,
Danie G. van Zyl
3   Department of Internal Medicine, University of Pretoria, South Africa
,
Paul Rheeder
4   Division of Clinical Epidemiology, University of Pretoria, Pretoria, South Africa
,
Johann C. Jerling
1   Department of Nutrition, North-West University, Potchefstroom, South Africa
,
John W. Weisel
5   Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
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Publikationsverlauf

Received 13. Juli 2006

Accepted after resubmission 06. September 2006

Publikationsdatum:
01. Dezember 2017 (online)

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Summary

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.