Abstract
The metabolic syndrome and type 2 diabetes are insulin-resistant states which are commonly associated with an atherogenic dyslipidaemia involving mild to moderately elevated triglycerides, a preponderance of small, dense low-density lipoprotein (LDL) particles and low levels of high-density lipoprotein cholesterol (HDL-C). In addition, there is a spectrum of qualitative changes in the lipoprotein profile, particularly in the functional capacity of HDL to facilitate cellular cholesterol efflux and to protect LDL against oxidative modification. Together, these quantitative and qualitative anomalies promote elevated oxidative stress, endothelial dysfunction and inflammation, which drive the development of premature atherosclerotic cardiovascular disease. Moreover, recent evidence indicates that this dyslipidaemic profile may play a critical role in the development and progression of diabetic microvascular disease. An integrated therapeutic approach to correct both the quantitative and qualitative changes characteristic of diabetic dyslipidaemia clearly constitutes a priority for reduction of both macrovascular and microvascular risk.