No abstract

Abstract-Triglyceride-rich lipoproteins (TRLs), namely chylomicrons (CMs), VLDL, and their remnants, are implicated in the atherogenic features of postprandial lipemia. In human plasma, cholesteryl ester transfer protein (CETP) mediates the heteroexchange of neutral lipids, ie, triglycerides (TG) and cholesteryl esters (CE), between distinct subpopulations of apoB-and of apoAI-containing lipoproteins. In fasting normolipidemic plasma, CETP plays an antiatherogenic role by promoting preferential CE redistribution from HDL to LDL particles of intermediate subclass with optimal binding affinity for the cellular LDL receptor. While the relative proportions and chemical compositions of donor and acceptor lipoproteins are known to influence CETP activity, elevated levels of TRL present during alimentary lipemia have been proposed to be associated with enhanced CETP activity. To identify the preferential CE acceptor particles among postprandial TRL subfractions, we investigated the effects of a typical Western meal (1200 kcal, 14% protein; 38% carbohydrate; and 48% fat, monounsaturated/polyunsaturated ratio 4:1) on the rates of postprandial CE transfer from HDL to apoB-containing lipoproteins in normolipidemic subjects (nϭ13). Two hours postprandially, plasma levels of TRL were significantly elevated (140 versus 51 mg/dL at baseline, Pϭ.0001). Total rates of CE transferred (88Ϯ7 g ⅐ h Ϫ1 ⅐ mL Ϫ1 ) from HDL to apoB-containing lipoproteins were not significantly modified by alimentary lipemia over a period of 8 hours. Quantitatively, LDL accepted 64Ϯ5 g CE per hour per milliliter plasma from HDL, whereas CM (SfϾ400), VLDL1 (Sf 60 to 400), VLDL2 (Sf 20 to 60), and IDL (Sf 12 to 20) accepted 5Ϯ3, 16Ϯ3, 1.4Ϯ0.3, and 1.5Ϯ0.2, respectively. Quantitatively, VLDL1 was the major CE acceptor among TRLs (Pϭ.0001); thus, VLDL1, but not CMs, represented the major CE acceptor among TRLs. Qualitatively however, VLDL2 and IDL displayed a higher capacity to accept CE from HDL (51.6Ϯ4.1 and 46.3Ϯ2.8 g CE transferred per hour per milligram lipoprotein, respectively; PϽ.005) compared with CM, VLDL1, and LDL (12.6Ϯ2.8, 34.7Ϯ4.2, and 22.7Ϯ2.0 g CE transferred per hour per milligram lipoprotein, respectively). In conclusion, elevated postprandial TRL levels are not associated with enhanced total CE transfer to these particles. Furthermore, the qualitative features of postprandial CE transfer from HDL to CM and VLDL1 were not related to the relative TG content of these particles. The CETP-facilitated enrichment of VLDL1 in CE therefore identifies them as potentially atherogenic particles during the postprandial phase. (Arterioscler Thromb Vasc Biol. 1998;18:65-74.)

The association of fats with carbohydrates results in a lower glucose response but the influence of the nature of the dietary fatty acids has not been investigated clearly. We examined the effect of the degree of dietary fatty acid unsaturation on the postprandial glucose and insulin responses to a mixed meal. Eight young normolipidemic men consumed four different meals in random order. The meals differed in the nature of their oils and in the type of their main carbohydrates. The meals contained either a high ratio of monounsaturated to polyunsaturated n-6 fatty acids (MUFA) or a low ratio (PUFA) and either potatoes or parboiled rice. Proteins and saturated and polyunsaturated n-3 fatty acid contents were not different among meals. Blood samples were collected every 30 min for 3 h after the test meal. The glucose response was significantly lower 30 min after the parboiled rice-PUFA meal than after parboiled rice-MUFA or potato-MUFA (P < 0.05) meals. The insulin response was lower after parboiled rice-PUFA than after potato-MUFA (P < 0.05) meals. Similarly, an effect of fat appeared after 30 min. Glucose responses (F = 1.4, P < 0.01) and insulin responses (F = 5.3, P < 0.05) to both carbohydrates were significantly lower with dietary PUFA compared with dietary MUFA. In conclusion, the degree of dietary fatty acid unsaturation (18:1 compared with 18:2) may influence the glucose and insulin responses to mixed meals.

The effects of dietary lipid and L-Met supplementation on plasma lipids and lipoproteins were investigated in 16-wk-old preruminant calves. Four calves received the basal milk diet (2.0 g of lipid/kg of BW per meal) for 8 d followed by the same diet supplemented with L-Met (2.6 g/kg of dietary DM) for 5 d. Similarly, seven calves received successively the basal diet supplemented with cream (2.7 g of lipid/kg of BW per meal) and the same diet supplemented with L-Met. The diet with cream induced higher triglyceridemia than the basal diet because of a marked increase in chylomicra and in very low density lipoproteins, which suggested stimulation of intestinal lipoprotein secretion. Moreover, this lipid-enriched diet stimulated the formation of very light high density lipoproteins to the detriment of heavy high density lipoproteins. These particles, the bovine counterpart of mammalian high density lipoproteins of type 1, were distributed within the density range of low density lipoproteins. Addition of L-Met in the diets increased plasma concentrations of chylomicra and very low density lipoproteins, suggesting direct stimulation of the intestinal secretion of both of these lipoproteins and of the hepatic very low density lipoproteins. No effect of L-Met was observed on the concentrations and the physicochemical properties of low and light high density lipoproteins.

Improving patient education, especially concerning their perception of risk, as well as increasing the involvement of dieticians, are motivators to explore in order to improve adherence.