A major cause for CVD risk is the atherogenic dyslipidemia that frequently precede the diagnosis of T2D by several years, indicating that the dyslipidemia is an early event in the development of cardiovascular complications of T2D. The dyslipidemia is characterized by elevated plasma concentration of both fasting and postprandial (i.e., after eating a meal) triglyceride-rich lipoproteins (TRLs), small dense LDL and low HDL cholesterol. Importantly this dyslipidemia is also common in general population in particular in obese subjects with insulin resistance and NAFLD.
The recent lessons from genetic studies have generated interest in raised concentrations of triglycerides and remnants. This renewed interest has been driven by both epidemiological and genetic evidence demonstrating that raised TRLs and their remnants are directly linked to increased CVD and all-cause mortality. Consequently, efforts to reduce the concentrations of both fasting and postprandial triglycerides and their remnants are critical to lessen the burden of residual risk in patients with heart disease.