Characterization of lipoprotein composition in rats fed different dietary lipids and of the effects of lipoproteins upon lymphocyte proliferation.
1996
Jeffery N.M. | Yaqoob P. | Wiggins D. | Gibbons G.F. | Newsholme E.A. | Calder P.C.
Weanling Lewis rats were fed for 10 weeks on a low fat (2.5% by weight; LF) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO); all other components of the diets were identical. The chylomicron (CM), very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) fractions were isolated from the serum. The serum from MO-fed animals had lower LDL and HDL cholesterol concentrations than the serum from animals fed each of the other diets. The apolipoprotein A-1 concentration in the HDL fraction from animals fed the MO diet was also low. The serum from HCO-fed animals had a higher CM triacylglycerol concentration than serum from animals fed each of the other diets. The serum from OO-fed animals had a higher VLDL triacylglycerol concentration than serum from animals fed each of the other diets. The concentration of apolipoprotein B was also high in the VLDL fraction from OO-fed animals. The fatty acid composition of each lipoprotein fraction was affected by the nature of the lipid in the diet; the greatest effects were observed in the CM and VLDL fractions. Each lipoprotein fraction isolated from LF-fed rats inhibited mitogen-stimulated rat spleen lymphocyte proliferation in a concentration-dependent manner; LDL and HDL caused greater inhibition than CM and VLDL. Dietary lipid manipulation did not alter the inhibitory effects of any of the lipoprotein fractions upon lymphocyte proliferation, except that CM and HDL from MO-fed animals and HDL from OO-fed animals resulted in enhanced proliferation compared with either CM or HDL from animals fed the other diets. We conclude that the inhibition of lymphocyte proliferation caused by feeding rats certain dietary lipids (OO, EPO, MO) may be mediated by non-lipoprotein serum components.
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