However, most of the existing animal models for investigating the role of hyperglycemia in atherosclerosis are genetically hypercholesterolemic mice (e. g., apolipoprotein E [apoE] or low-density lipoprotein receptor-deficient mice), in combination with streptozotocin-induced pancreatic β-cell destruction or crossbreeding with genetically obese diabetic mice [24,25]. This evidence concerns the gene VLDLR and atherosclerosis.