Diabetic patients are at increased risk of developing dyslipidaemia. One mechanism underlying this connection is increased free fatty-acid release present in insulin-resistant fat cells. High levels of free fatty acids promote triglyceride production, which in turn stimulates the secretion of Apo lipoprotein B (ApoB) and very LDL (VLDL) cholesterol. High levels of ApoB and VLDL have both been tied to increased risk of CVD. In addition to high ApoB and VLDL, hyperinsulinemia is associated with low high-density lipoprotein (HDL) cholesterol levels. Hyperglycaemia may also negatively impact lipoproteins (particularly LDL and VLDL) through increased glycosylation and oxidation, decreasing vascular compliance and facilitating the development of aggressive atherosclerosis. High circulating FFA’s and triglycerides, increased stimulation of ApoB and VLDL cholesterol, decreased HDL levels and lipoprotein modification have all been appreciated in patients with DM and likely contributes to the high prevalence of CVD in diabetic patients.

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