The accumulation of macrophages in the intima of the aorta found in our TEM investigation may be, as Quinn showed in her study, the consequence of hyperglycemia that stimulates the low density lipoprotein (LDL) glycation, process that makes them miss the connection with LDL receptors, leading to the cholesteryl esters synthesis, a mechanism that attracts the macrophages to uptake these lipid molecules and to develop the foam cells [2]. Here, LDLR is linked to Hyperglycemia.