Glycated apolipoprotein B-A surrogate marker of subclinical atherosclerosis

Sustained hyperglycemia is a causative factor for glycation of proteins. Glycated low-density lipoprotein (LDL) is strongly associated with an increased risk of CAD (Coronary Artery Disease) in diabetics. Hence, we planned to evaluate the association of glycated apo B with subclinical atherosclerosis.

Forty-five non obese and 45 obese diabetics were recruited. Glycated hemoglobin (HbA1c) levels were estimated by HPLC (High Pressure Liquid Chromatography) and small dense low-density lipoprotein (sdLDL) was calculated using standard formula. Plasma Insulin was done by RIA. Insulin resistance was calculated using homeostatic model assessment insulin resistance (HOMA-IR) model. Glycated apo B in serum was estimated using ELISA. Carotid intimal media thickness (CIMT) was estimated using B mode USG of carotid arteries.

Glycated apo B levels were correlated significantly with fasting blood glucose (FBG) (p=0.001), post prandial glucose (PPG) (p=0.001), HbA1c (p=0.013). The percent glycated apo B levels correlated significantly with FBG (p=0.032), PPG (p=0.004) in obese diabetic group. Multivariate regression analysis of glycated apo B and percent glycated apo B, showed that glycated apo B (p=0.009) and percent glycated apo B (p=0.006) were significantly correlated to FPG in diabetic population. The percent glycated apo B was also significantly correlated to PPG (p=0.003) and sdLDL (p=0.009). CIMT levels were higher in obese diabetics with 2 plaques positive when compared to obese non diabetic controls; however levels were not statistically significant.

Persistent hyperglycemia and sdLDL are independently associated with glycation of apo B. Presence of plaques and increased thickness of intima indicates that glycated apo B predisposes diabetics to atherosclerosis.