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Patients with diabetes often present with abnormal lipid profiles because insulin regulates several of the steps of lipid metabolism. Patients with type 1 diabetes that exhibit effective glycaemic control do not have quantitative lipoprotein abnormalities, but may exhibit qualitative abnormalities, mainly an increase in smaller, more atherogenic very low-density lipoprotein (VLDL) particles. Furthermore, in the Diabetes Control and Complications Trials (DCCT) study, the group of patients with type 1 diabetes that were characterised by consistent weight gain, exhibited lipid profiles more typical of type 2 diabetes (T2D). Dyslipidaemia in T2D is characterised by several strictly linked abnormalities: elevated fasting and postprandial triglycerides (TG), a significant decrease in high-density lipoprotein (HDL) cholesterol and an increase in smaller low-density lipoprotein (LDL) and HDL particles. The increase in plasma TG is largely explained by the increased production of TG-rich; large-sized VLDL in particular. The insulin resistant liver fails to inhibit lipid attachment to pre-VLDL molecules and synthesises larger-sized VLDL at a greater rate. Large TG-rich; VLDL enhances the transfer of core lipids between VLDL, LDL, and HDL with increased formation of smaller LDL and HDL. Also, the elevated postprandial TG that are often present in patients with T2D may be linked to insulin resistance. Therefore, the abatement of hyperglycaemia and insulin resistance should be one of the main treatment objectives to address dyslipidaemia in patients with diabetes. [ABSTRACT FROM AUTHOR]