Postprandial lipoproteins in non-insulin-dependent diabetes mellitus

People with non-insulin-dependent diabetes mellitus (NIDDM) have a higher incidence of cardiovascular disease (CVD) than the non-diabetic population. In addition, NIDDM patients have a spectrum of lipid abnormalities that may confer an increased risk of developing CVD. The pattern of dyslipidaemia seen in NIDDM patients is different from that seen in the non-diabetic population. This suggests that patients with NIDDM may need different lipid-lowering treatment from that used in the non-diabetic population. In the post-absorptive state, secretion of very low-density lipoprotein (VLDL) is higher in patients with NIDDM, possibly because of the impaired ability of insulin to inhibit lipolysis and to reduce hepatic VLDL secretion. Clearance of triglyceride-rich lipoproteins is also important in determining the extent of postprandial hyperlipidaemia. Lipoprotein lipase (LPL) reduces plasma lipoprotein concentration via several mechanisms. In patients with NIDDM, the capacity of LPL to minimize postprandial hyperlipidaemia may be reduced, although the pathophysiological basis of this is not known. Other changes in patients with NIDDM, such as modifications to cholesteryl ester transfer protein (CETP) and hepatic lipase activity, may also affect postprandial lipaemia but such effects are probably secondary to alterations in lipoprotein clearance. Present evidence suggests that postprandial hyperlipidaemia is atherogenic. There are, however, little specific data from patients with NIDDM. More studies are therefore needed to establish the optimal treatment of dyslipidaemia in patients with NIDDM.