It has therefore been hypothesized that in insulin resistance associated with hyperglycemia, as in type 2 diabetes, insulin no longer represses APOC3 expression, whereas chronic glucose elevation enhances APOC3 expression, leading to increased plasma apoC-III levels and increased risk for atherosclerosis, via either induction of hypertriglyceridemia or other vascular effects of apoC-III [30, 52]. This evidence concerns the gene APOC3 and Hyperglycemia.