Fish oil supplementation reduces beta-very low density lipoprotein in type III dysbetalipoproteinemia.

Abstract

0-Very low density lipoproteins (^J-VLDLs) are atherogenic, cholesterol-rich chylomicron and VLDL remnants that accumulate in the plasma of type III dysbetalipoproteinemic subjects. To evaluate the effect offish oil supplementation on plasma /3-VLDL concentrations, we compared the lipid and lipoprotein responses in nine type III and nine type IV hyperlipidemic subjects. Each individual received 6 g/day o>-3 fatty acids for 12 weeks. Before treatment, the mean total cholesterol, total triglyceride, VLDL triglyceride, low density lipoprotein (LDL) cholesterol, and high density lipoprotein (HDL) cholesterol levels were not different between groups. Conversely, VLDL cholesterol, intermediate density lipoprotein (IDL) cholesterol, and IDL triglycerides were higher in type III than in type IV subjects. Fish oil supplementation was associated with significantly lower levels of cholesterol (-50%), triglycerides (-50%), and apolipoprotein B (-50%) in the d< 1.006 g/ml ultracentrifugation plasma fraction in both groups, compatible with a reduction in VLDL in type III and type IV subjects, and in /3-VLDL in type III subjects. This finding was confirmed by analysis of the plasma zonal ultracentrifugation profile and the agarose gel electrophoretic pattern of lipoproteins, which showed a reduction in but not a disappearance of remnant particles, suggesting that not all /3-VLDL had been cleared after treatment. The levels of IDL cholesterol and IDL triglycerides (1.006<d< 1.019 g/ml) were not affected in either group. Initially low LDL cholesterol (1.019 <d< 1.063 g/ml) and HDL cholesterol levels rose significantly in both groups. In type III hyperlipidemics, all LDL cholesterol values remained below 120 mg/dl, whereas they were higher than 150 mg/dl after treatment in two individuals with type IV hyperlipidemia. In conclusion, our results demonstrate that fish oil supplementation is equally effective in lowering total triglycerides and triglycerides in the d< 1.006 g/ml plasma fraction in type III and type IV hyperlipidemias. In addition, fish oils reduce chylomicron and VLDL remnant concentrations in type HI dysbetalipoproteinemia. {Arteriosclerosis and Thrombosis 1991;11:864-871) T ype III dysbetalipoproteinemia is a lipid disorder characterized by the accumulation in plasma of cholesterol-rich very low density lipoproteins (VLDLs), that is, /3-VLDL.1 These heterogeneous lipoproteins are made up of remnants of both hepatic and intestinal origin.

Influence of probucol on enhanced LDL oxidation after fish oil treatment of hypertriglyceridemic patients.

“…5 Both groups responded to 6 g/d of n-3 fatty acids with an approximate 50% decrease in very-low-density lipoprotein (VLDL) triglyceride (TG), similar to that observed in other studies conducted in various population samples. In some individuals, especially type IV hypertriglyceridemic patients, a significant increase in LDL cholesterol was noted.…”

“…In some individuals, especially type IV hypertriglyceridemic patients, a significant increase in LDL cholesterol was noted. 5 For several patients, however, the diet-fish oil therapeutic combination appeared to be a satisfactory alternative to more classic drug therapy. The current study was undertaken to assess lipid peroxidation and the susceptibility of LDL to in vitro oxidation during dietary supplementation with fish oil in hyperlipidemia.…”

Fish oil and cardiovascular disease: lipids and arterial function

“…Chylomicronemia after a fatty meal is diminished when fish oil is eaten over 2 wk (2) but not after a single meal. Remnants in type 3 hyperlipoproteinemia are partly cleared with fish-oil treatment (3).…”

Lack of Triglyceride-Lowering Properties of Fish Oil in Apolipoprotein E–Deficient Mice

“…5,6 Fish oil decreases the plasma concentration of VLDL and chylomicron remnants in patients with dysbetalipoproteinemia. 7 The decreased hepatic TG synthesis usually induced by a fish oil diet certainly contributes to a reduction in the formation of TG-rich lipoproteins (TRLs) and their remnants. Alternatively, lower amounts of TRLs reduce the amount of lipoproteins that compete with remnants for receptormediated clearance, therefore promoting remnant uptake.…”