Fibrinogen glycation and glycaemic control in type 2 diabetic subjects / L.T. Göttsche.
Göttsche, Louise Theresia
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Type 2 diabetes mellitus is a worldwide pandemic that causes both micro- and macrovascular complications. Although the causal relationship between chronic hyperglycaemia and microvascular disease have been established, the relationship between chronic hyperglycaemia and macrovascular disease (including cardiovascular disease (CVD)) is not yet well defined. A possible causal mechanism may be related to the glycation of haernostatic proteins such as fibrinogen. Hyperglycaemia causes non-enzymatic glycation of proteins through direct binding of carbohydrates (glucose and to a minor extent fructose) to proteins. The results of this study indicated that uncontrolled African type 2 diabetic subjects had a significantly higher level of fibrinogen glycation than non-diabetic subjects and that achievement of glycaemic control indeed resulted in a significant decrease in fibrinogen glycation. Glycated fibrinogen also correlates with and compares well with HbAlc in monitoring glycaemic control. By correlating end fibrinogen glycation levels with the average fasting capillary glucose of different 4-day time- intervals (fibrinogen has a half-life of 4 days) the study indicated that fibrinogen could be used as a short-term indicator of glycaemic control. Because fibrinogen is involved in vascular disease itself, glycated fibrinogen may be a better long-term predictor of CVD than current markers of glycaemic control. It may also aid in the elucidation of the relationship between hyperglycaemia and CVD. The results of this study showed that fibrinogen glycation is indeed sensitive to fluctuations in glycaemic control.
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