The prevalence of hypercholesterolaemia is similar in non-insulin-depe
ndent diabetic (NIDDM) patients and in non-diabetic subjects. The prev
alence of hypertriglyceridaemia and of low high-density-lipoprotein (H
DL) cholesterol is roughly double the norm in NIDDM, but the exact pre
valence varies greatly from study to study. Obesity and a familial for
m of hypertriglyceridaemia (conditions that may alter plasma lipoprote
in levels) are frequently observed in NIDDM patients. In carefully con
trolled NIDDM patients without concomitant primary hyperlipoproteinaem
ia, body weight may be more important than glycaemic control or the ty
pe of treatment plan adopted in determining lipoprotein levels. Hypert
riglyceridaemia in NIDDM is a result of both increased very-low-densit
y-lipoprotein (VLDL) synthesis and impaired VLDL catabolism. Whilst lo
w-density-lipoprotein (LDL) levels are normal, the LDL synthesis and r
emoval rates may be increased. Low high-density-lipoprotein (HDL) leve
ls may be due to increased catabolism. In addition to quantitative cha
nges in plasma lipids and lipoproteins, NIDDM patients demonstrate qua
litative lipoprotein alterations. The size and density of LDL particle
s in NIDDM patients are greatly affected by triglyceride levels. Small
er, denser LDL particles have been observed in hypertriglyceridaemic s
ubjects. Glycosylation of apolipoproteins may alter the metabolic prop
erties of lipoproteins. Glycosylated and small, dense LDL have an incr
eased susceptibility to oxidation.