Pieters Marlien, Covic Namukolo, Loots Du Toit, van der Westhuizen Francois H, van Zyl Danie G, Rheeder Paul, Jerling Johann C, Weisel John W
Department of Nutrition, North-West University, Potchefstroom Campus, Private Bag X6001, Potchefstroom, 2520 South Africa.
Thromb Haemost. 2006 Nov;96(5):623-9.
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.
糖尿病患者已被证明存在纤维蛋白网络结构改变。一个可能的原因可能是纤维蛋白原糖基化导致结构/功能特性改变。我们研究了血糖控制对2型糖尿病患者纤维蛋白原糖基化和纤维蛋白网络结构的影响。在基线时从20名血糖未得到控制的糖尿病患者采集血样，以测定纤维蛋白原糖基化水平和纤维蛋白网络结构。然后对这些患者用胰岛素进行治疗，直至实现血糖控制，之后采集终末血样。纳入20名年龄和体重指数匹配的非糖尿病患者作为参照组。糖尿病患者在基线时的平均纤维蛋白原糖基化水平显著高于非糖尿病患者（7.84对3.89摩尔葡萄糖/摩尔纤维蛋白原；p<0.001）。在糖尿病组干预期间，这一水平显著降低（从7.84降至5.24摩尔葡萄糖/摩尔纤维蛋白原；p<0.0002）。两组的平均纤维蛋白原浓度均较高（糖尿病患者和非糖尿病患者分别为4.25和4.02 g/l）。在基线时，糖尿病患者和非糖尿病患者之间在纤维蛋白原浓度、孔隙率、紧实度和凝块形成动力学方面没有差异，尽管纤维蛋白原糖基化有所降低，但在干预期间也没有任何变化。纤维蛋白网络特征与纤维蛋白原密切相关，但与任何血糖控制指标均无关。血糖控制改善导致纤维蛋白原糖基化降低，但纤维蛋白原浓度未降低。在该模型中，似乎孔隙率、紧实度和凝块形成动力学与纤维蛋白原浓度的关系比与纤维蛋白原糖基化的关系更大。
