Atherosclerosis is a major complication of diabetes, increasing the risk of cardiovascular related morbidities and mortalities. The hallmark of diabetes is
hyperglycemia which duration is best predicted by elevated glycated haemoglobin A1C (HbA1C) levels.
Diabetic complications are usually attributed to oxidative stress associated with glycation of major structural and functional
proteins. This non-enzymatic glycation of long lived
proteins such as
collagen,
albumin,
fibrinogen, liver
enzymes and
globulins result in the formation of early and
advanced glycation end products (AGEs) associated with the production of myriads of free radicles and
oxidants that have detrimental effects leading to
diabetic complications. AGEs have been extensively discussed in the literature as etiological factors in the advancement of atherogenic events. Mechanisms described include the effects of glycation on
protein structure and function that lead to defective receptor binding, impairment of immune system and
enzyme function and alteration of basement membrane structural integrity.
Hemoglobin (Hb) is a major circulating
protein susceptible to glycation. Glycated Hb, namely HbA1C is used as a useful tool in the diagnosis of diabetes progression. Many studies have shown strong positive associations between elevated HbA1C levels and existing
cardiovascular disease and major risk factors. Also, several studies presented HbA1C as an independent predictor of cardiovascular risk. In spite of extensive reports on positive associations, limited evidence is available considering the role of glycated Hb in the etiology of
atherosclerosis. This editorial highlights potential mechanisms by which
glycated hemoglobin may contribute, as a causative factor, to the progression of
atherosclerosis in diabetics.