The Journal of Nutrition Vol. 128 No. 3 March 1998, pp. 582-586

An NCEP II Diet Reduces Postprandial Triacylglycerol in Normocholesterolemic Adults¹²

Michael Miller^{*, 3}, Beverly Teter, Christina Dolinar^*, and Angeliki Georgopoulos^**

^* VA and University of Maryland Medical Center, Baltimore, MD 21210,  University of Maryland at College Park, College Park, MD 20742 and ^** VA and University of Minnesota, Minneapolis, MN 55455

	ABSTRACT

Abstract Introduction Methods Results Discussion References

We compared the fasting and postprandial response to a National Cholesterol Education Program (NCEP) II diet with that of a diet high in total (40% of energy) and saturated fat. In free-living conditions, 17 healthy normolipidemic, normoglycemic men and women consumed a high-fat diet, a maintenance diet and the NCEP II diet, for 1 mo each. At the completion of each dietary period, an oral fat load (70 g/m² body surface area) was administered and plasma triacylglycerol (TAG) determined every 2 h for 8 h. Compared with the high-fat phase, the NCEP II diet was associated with significantly lower energy intake (12.1 ± 1.1 vs. 7 ± 0.7 MJ/d) and final body weight (78 ± 3.8 vs. 76.3 ± 3.5 kg) (P < 0.01). Plasma high density lipoprotein cholesterol, apolipoprotein (apo) A-I and ApoB concentrations were also significantly lower when subjects consumed the NCEP II diet rather than the high-fat diet (P  0.004). There were no significant differences in subjects fasting TAG, glucose or insulin concentration between the high fat and NCEP II diet periods. However, the postprandial plasma TAG response to the fat load was lower after completing the NCEP II than after the high-fat diet period (P = 0.045). Under free-living conditions, a NCEP II diet was associated with weight loss and a decrease in postprandial but not fasting TAG. Because dietary alteration may not affect fasting TAG levels, thorough assessment of a dietary intervention should include measurements of postprandial TAG.

	INTRODUCTION

Abstract Introduction Methods Results Discussion References

It has been hypothesized that atherogenesis is a postprandial phenomenon (Zilversmit 1995) and that valuable information may be obtained by evaluating the triacylglycerol (TAG)⁴-rich lipoprotein response to a fat load (Ebenbichler et al. 1995). In normocholesterolemic subjects consuming a meal high in fat, there is an initial peak of TAG that appears in plasma 2-4 h postprandially with an occasional secondary peak several hours later (Heller et al. 1993). The early peak reflects TAG-rich lipoproteins that are predominantly of intestinal origin, whereas, the latter peak is derived primarily of hepatically synthesized TAG particles (Cohn et al. 1989). An abnormal response to a fat load characterized by higher TAG peaks or delayed clearance may accelerate atherogenesis by facilitating uptake and incorporation of TAG-rich lipoproteins by macrophages (Gianturco and Bradley 1988); this pattern has been reported in certain dyslipidemias associated with premature coronary artery disease (CAD) (Ooi et al. 1992).

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

Although studies have contrasted dietary fat intake and its relative impact on lipoprotein levels (Brussaard et al. 1980, Grundy and Denke 1990) and CAD (Blankenhorn et al. 1990), there have been no studies in normocholesterolemic subjects specifically evaluating whether differential responses to a fat load occur after consumption of a high- or low-fat diet. This information may be particularly useful because although lipid and lipoprotein measurements are assessed most often in the fasting state, the majority of each day is spent in the postprandial state. We hypothesized that an NCEP II diet might beneficially alter the postprandial response to fat in normocholesterolemic subjects compared with a diet high in total and saturated fat. An outpatient rather than metabolic ward setting was chosen to simulate conditions more similar to the free-living state.

	MATERIALS AND METHODS

Abstract Introduction Methods Results Discussion References

Subjects.  Subjects were eligible to participate if they were free of systemic illness, normolipidemic [total cholesterol (TC) < 6.2 mmol/L (240 mg/dL), TAG < 2.82 mmol/L (250 mg/dL)] and were not receiving lipid-altering medications. The ranges for entry were TC, 3.64-5.84 mmol/L; TAG, 0.46-2.72 mmol/L. Seventeen subjects (11 men and 6 women) successfully completed the study during a 2-y period. The mean age of the participants was 33.8 ± 4.6 y.

Study protocol.  Informed consent was obtained from the Institutional Review Boards at The University of Maryland Medical Center and The Johns Hopkins Hospital. Dietary instruction was provided by a registered dietician; subjects initially were fed a "high-fat" diet and were instructed to consume 40% of their energy needs from fat. The high-fat phase was initiated intentionally during the winter holiday season because all participating subjects acknowledged a high degree of compliance to a diet high in total and saturated fat during this period. After completion of this 1-mo phase, each subject had blood drawn for various measurements (see further) after an overnight fast of 12 h. Subjects then were administered a "milkshake" or fatty meal consisting of corn oil [70 g/m² body surface area (BSA)], mixed with skim milk and Sweet and Low® (Cumberland Packing, Brooklyn, NY) that was flavored with strawberry or vanilla. The energy intake for the "milkshake" was 6.9 mJ derived primarily from corn oil (86.3%) with smaller contributions from carbohydrate (8.1%) and protein (5.6%). Subjects were asked to consume the "milkshake" during a 10- to 15-min period after which time blood was collected in EDTA containing tubes via multiple sticks every 2 h for a total of 8 h. Blood was placed immediately in wet ice and centrifuged at 2000 × g for 10 min at 4°C. At each time point, plasma was stored in aliquots at either 4 or 70°C for various measurements (see further). During the 8-h interval after consumption of the milkshake, subjects were asked to remain sedentary and not to consume any food. Water was permitted and encouraged during the study period.

Upon completion of the first dietary phase, subjects returned to their usual diet for 1 mo (maintenance period). During the 3rd mo of the study, they received National Cholesterol Education Program (NCEP) Step II dietary instruction to consume <200 mg of dietary cholesterol, 55% of energy from carbohydrates, 15% of energy from protein and <7% of total energy in saturated fat daily. Upon completion of this phase, the same oral fat load was administered and blood was sampled at the same time intervals (0, 2, 4, 6 and 8 h) as performed for the high-fat phase.

In an effort to maximize dietary compliance, the dietician recommended food products that each subject enjoyed consuming. Therefore, some subjects may have derived a higher percentage of saturated fat from cheese, whereas others consumed more ice cream. Subjects reported adhering to each assigned diet, and the fat meal was tolerated without untoward side effects. The last nine subjects entering the study completed 72-h dietary records during the final week of each of the respective dietary phases.

Lipoprotein and biochemical analysis.  Lipids, lipoproteins and apolipoproteins (apo) were measured in the blood drawn at specific time points as described below. Enzymatic measurement of cholesterol (C) and TAG was performed on a Hitachi 704 clinical chemistry analyzer (Boehringer Mannheim Diagnostics, Indianapolis, IN) with reagents supplied by the manufacturer. High-density lipoprotein-C (HDL-C) was determined after precipitation of apoB-containing lipoproteins with heparin sulfate and manganese chloride using the method of Warnick and Albers (1978). Low-density lipoprotein-C (LDL-C) was estimated using the formula established Freidewald et al. (1972). Apo A-I and B were measured by radial immunodiffusion (apo A-I, Tago, Burlingame, CA; apo B, Behring Diagnostics, Somerville, NJ). Lipoprotein (a) [Lp(a)] was measured with a commercially available enzyme-linked immunosorbent assay (Terumo, Elkton, MD). All measurements were performed at The Johns Hopkins Lipoprotein Analytical Laboratory, a laboratory standardized by the Centers for Disease Control-National Heart, Lung and Blood Institute Lipid Standardization Programs (Myers et al. 1989). Glucose measurements were performed by the direct hexokinase method of Neese (1982), and insulin levels were assessed by the microparticle enzyme immunoassay (Fiore et al. 1988). Apo E phenotyping was performed at the Medlantic Research Foundation (Washington, DC).

Analysis of plasma fatty acids.  In six of nine subjects who maintained 72-h dietary records, an extra aliquot of plasma (maintained at 70°C) was collected to analyze total fatty acid composition. To each sample (~0.5 mL plasma), 0.3 mL methylene chloride was added as cosolvent and then 2 mL anhydrous methanolic:HCl (1 mol/L) was added and refluxed overnight at 80°C. Samples were extracted thrice using hexane (2 mL) after the addition of KCl (2 mL) and water (1 mL) and centrifuged. The organic layer was dried under N₂, redissolved in hexane and passed through a silicic acid mini-column. The semi-purified methyl esters were dissolved in isooctane and analyzed using a HP 5890 gas chromatograph (Sampugna et al. 1982).

Statistical analysis.  Food records were analyzed by a registered dietician using Nutritionist-3 Program (N-squared Computing, Salem, Oregon). Differences in energy intake, lipid, lipoprotein and various biochemical measurements during the high-fat and NCEP II dietary phases were assessed by paired two-tailed t test. In cases of nonparametric testing, the Wilcoxon rank sum test was used. Analysis of plasma fatty acids was performed using the GLM procedure of the SAS system. The dietary differences with respect to plasma postprandial TAG were assessed by repeated measures analysis of variance ANOVA (Winer 1971). The designated level of significance is P < 0.05.

	RESULTS

Abstract Introduction Methods Results Discussion References

The last nine subjects enrolled in the study completed 72-h food records during each of the dietary phases (Table 1). The total energy intake and cholesterol consumed was significantly higher during the high-fat dietary phase. Analysis of food records disclosed adherence to the high-fat diet but greater restriction in total fat intake than instructed during the NCEP II dietary phase. This resulted in significantly lower amounts of saturated and monounsaturated fat and correspondingly higher levels of polyunsaturated fat intake. There were no significant differences in energy intake between the run-in (10.3 ± 0.9 MJ) and maintenance (8.3 ± 0.6 MJ) periods. Similarly, no differences were observed in energy intake resulting from either alcohol ingestion or simple sugars between the run-in (0.05 ± 0.02 MJ, 0.5 ± 0.1 MJ) and maintenance (0.05 ± 0.02 MJ, 0.3 ± 0.1 MJ) periods compared with the high-fat and NCEP II dietary periods (Table 1).

Dietary compliance also was assessed by quantifying plasma free fatty acids (FFA) in six of the nine subjects completing 72-h dietary recall records (Table 2); samples were insufficient to perform the FFA assay in the remaining three subjects. Subjects had significantly lower levels of 18:1 trans fatty acids in plasma during the NCEP II diet phase than during the high fat phase (P = 0.017).

Table 3 lists the clinical and biochemical measurements for each subject at the conclusion of the two dietary phases. None of the study subjects were homozygous for the Apo E₂ or E₄ allele. When subjects consumed the NCEP II diet, they had significantly lower mean weights and HDL-C levels than when they consumed the high-fat diet (P  0.01). There were no significant differences in fasting total C, TAG or LDL-C between the high fat and NCEP II dietary periods. Lipid and lipoprotein measurements were not different between men and women during the high-fat and NCEP II dietary phases (data not shown).

A comparison between mean fasting and postprandial measurements of apolipoproteins A-I and B, Lp(a), glucose and insulin after completion of the diet phases is shown in Table 4. Moreover, fasting levels of apo A-I and apo B were significantly lower after subjects consumed the NCEP II diet (P < 0.01). These differences were maintained throughout the postprandial phase. There were no differences in fasting or postprandial levels of Lp(a) between the high fat and NCEP II diet phases. Fasting glucose concentrations tended to be lower during the NCEP II compared with the high-fat diet period (P = 0.09), but these alterations were attenuated during the postprandial phase. There were no significant differences in insulin levels at baseline or during the postprandial phase among the 13 subjects who had measurements performed when fasting.

The postprandial TAG response to a fat load is shown in Figure 1. Although there were no differences in fasting TAG between the high-fat and NCEP II dietary phases, the NCEP II diet was associated with an overall lower plasma TAG response (2, 4, 6 and 8 h) compared with the high saturated fat diet (P = 0.046, repeated measures ANOVA).

View larger version (11K): [in this window] [in a new window]   Fig 1. Assessment of the postprandial response of plasma triacylglycerols (TAG) to a fat load in fasting men and women who had consumed a high fat () or NCEP II diet (···) for 1 mo before the fat load. Values are means ± SEM, n = 17. The postprandial TAG response was significantly different between the two groups (P = 0.046, repeated measures analysis of variance).

	DISCUSSION

Abstract Introduction Methods Results Discussion References

The most important finding in this study was that compared with a diet high in total and saturated fat, the NCEP II diet reduced the postprandial plasma TAG response to a fat load. During this low-fat phase, the mean fat intake reported was considerable more stringent than the official recommendations outlined by NCEP. The significant weight differential between the dietary phases is also consistent with overadherence to a very low-fat diet rather than underreporting of fat in dietary food records. Although 72-h dietary records were available only in nine of the subjects, all participants were counseled similarly on the high fat and NCEP II diet; furthermore, there were no differences in weight alterations or postprandial responses between the subjects who did or did not complete 72-h food diaries. In general, decreased energy consumption resulting from reduced total and saturated fat intake leads to weight loss and affects lipids and lipoproteins in hyperlipidemic subjects (Lichtenstein et al. 1994).

The reported mean energy intake was not different between the 72-h baseline assessment and high-fat diet phase (10.3 ± 0.9 vs. 12.1 ± 1.1 MJ/d; P = 0.19). In contrast, significant reductions in mean energy intake were observed during the maintenance period (12.1 ± 1.1 vs. 8.3 ± 0.6 MJ/d; P = 0.005) with an associated mean weight loss of 1.9 kg. These differences persisted through the NCEP II dietary phase (8.3 ± 0.6 vs. 7.0 ± 0.7 MJ/d; P = 0.04). Consistent with imposed dietary fat restriction were significant reductions in HDL-C, apo A-I and apo B; this may be reflective of reduced synthesis of these particles (Shepherd et al. 1982). However, we cannot exclude the possibility that enhanced catabolism may have contributed in part to the results obtained because radiolabelled studies were not performed. Conversely, although the overall percentage of plasma total fatty acids was not disparate between the high-fat and NCEP II phases among the six subjects analyzed, there were significant increases in 18:1 trans-fatty acids during the high-fat phase. However, it is unlikely that the small differences observed (1%) affected lipid or lipoprotein levels in the present study. Finally, the lack of a reduction in the saturated fatty acid content might be related to enhanced endogenous saturated fatty acid synthesis on the NCEP II diet (Hudgins et al. 1996).

Associated with reduced total and saturated fat intake in the NCEP-II-treated phase were significant reductions in apo B levels without marked alteration in LDL-C. A previous study by Grundy et al. (1986) showed that more extreme reductions in total and saturated fat intake were not associated with further reduction in LDL-C. That apo B concentrations were lowered significantly during the NCEP II phase suggests that compositional (rather than mass) changes occurred in LDL-C, producing more buoyant and presumable less atherogenic particles (Austin et al. 1988).

In normolipidemic subjects, fasting TAG does not necessarily predict the postprandial TAG response as suggested by Nestel (1964), Cohn et al. (1988) and Lewis et al. (1991). Although isocaloric substitution of fat for carbohydrates often results in elevation of TAG due to enhanced hepatic very low-density lipoprotein-(VLDL-C) production (Weisweiler et al. 1985), the reduced energy intake during the NCEP II diet phase may have offset any potential TAG elevation caused by an increased carbohydrate intake (Table 1). Thus although participants were instructed to maintain similar energy intakes with substitution of carbohydrate for fat, the mean body weights were lower during the low (compared with high)-fat phase, precluding an accurate determination as to the relative contributions of weight and fat consumption in causing the divergent postprandial effects. Metabolic ward studies (Jackson et al. 1984, Wardlaw and Snook 1990), by contrast, although rigidly controlling for all dietary elements to minimize significant changes in body weight, are limited in their generalizability to freeliving subjects. Indeed, the present study may be more generalizable to clinical practice where dietary recommendations often favor a restricted fat diet (and the potential for associated weight loss) rather than advocating the equivalent energy intake derived from carbohydrates in place of fat.

We also evaluated the effect of the two high-fat and NCEP II diets on fasting and postprandial insulin and glucose concentrations. Although these indices are altered in patients with noninsulin dependent diabetes mellitus (Hollenbeck and Coulston 1991), limited information is available in normocholesterolemic, normoglycemic subjects. In contrast to the observed differences in the TAG response to fat ingestion, there were no differences between fasting and postprandial glucose and insulin levels.

Limitations of the present study include the lack of randomization of the dietary periods. Another possible factor could be seasonal variability (Buxtorf et al. 1988). The study was conducted in the winter holiday season (December-February) during which all subjects who, under basal conditions, did not consume a high-fat diet, were more likely to comply to a seasonal high-fat diet. Indeed, a diet high in total and saturated fat is more common in Americans during this period and simulates free-living conditions. However, the study was completed by late winter, suggesting that seasonal variability did not influence our findings. The results of the present study are also consistent with previous outpatient studies in free-living hypercholesterolemic subjects where the NCEP diet was associated with significant reductions in both energy intake and weight (Davidson et al. 1996, Walden et al. 1997). There were no alterations in fasting TAG observed in these studies; postprandial TAG measurements were not assessed.

In conclusion, the present study demonstrates that compared with a high-fat diet, the NCEP II diet decreases the postprandial TAG response to a fat load in normocholesterolemic adults without adversely affecting fasting TAG levels. One possible explanation for the greater fat tolerance with a low-fat diet in the absence of a fasting TAG change may relate to synthesis of endogenous TAG from enhanced endogenous fatty acid synthesis (especially palmitate) as a consequence of carbohydrate induction (Hudgins et al. 1996). Increases in lipoprotein lipase (LPL) activity, in association with weight reduction and heightened insulin sensitivity also might explain greater postprandial TAG removal. Unfortunately, LPL activity was not measured. We do not believe insulin resistance was a factor because glucose and insulin concentrations did not differ appreciably during the high-fat and NCEP II phases (Table 4). Nonetheless, whether the results obtained in the present study reflect weight loss alone as suggested by Lichtenstein et al. (1994), reduction in fat intake (total and saturated) or a proportional contribution of the two variables is unknown and warrants further investigation. Regardless, these data suggest that postprandial lipoprotein measurements provide information on the effects of dietary alterations that could differ from those obtained from fasting TAG measurements alone. Therefore, given the relationship between postprandial TAG and CAD (Patsch et al. 1992), it would be of interest to examine the postprandial effect of an NCEP II diet in subjects at risk for premature CAD.

	ACKNOWLEDGMENTS

Computational assistance was received from the CDMAS of the General Clinical Research Center of The Johns Hopkins University School of Medicine sponsored by National Institutes of Health Grant RR-00035.

	FOOTNOTES

Manuscript received 23 June 1997. Initial reviews completed 9 August 1997. Revision accepted 13 November 1997.

	LITERATURE CITED

Abstract Introduction Methods Results Discussion References

• Austin M. A., Breslow J. L., Hennekens C. H., Buring J. E., Willett W. C., Krauss R. M. Low-density lipoprotein subclass patterns and risk of myocardial infarction. J. Am. Med. Assoc. 1988; 264:3047-3052
• Barr S. I., Kottke B. A., Mao S.J.T. Postprandial distribution of apolipoproteins C-II and C-III in normal subjects and patients with mild hypertriglyceridemia: comparison of meals containing corn oil and medium-chain triglyceride oil. Metabolism 1985; 34:983-992 [Medline]
• Blankenhorn D. H., Johnson R. L., Mack W. J., El Zein, H. A., Vailas L. I. The influence of diet on the appearance of new lesions in human coronary arteries. J. Am. Med. Assoc. 1990; 263:1646-1652 [Abstract]
• Brussaard J. H., Dallinga-Thie G., Groot P.H.E., Katan MB. Effects of amount and type of dietary fat on serum lipids, lipoproteins and apolipoproteins in man: a controlled 8-week trial. Atherosclerosis 1980; 36:515-517 [Medline]
• Buxtorf J. C., Baudet M. F., Martin C., Richard J. L., Jacotot B. Seasonal variations of serum lipids and apolipoproteins. Ann. Nutr. Metab. 1988; 32:68-74 [Medline]
• Cohn J. S., McNamara J. R., Cohn S. D., Ordovas J. M., Schaefer E. J. Postprandial plasma lipoprotein changes in human subjects of different ages. J. Lipid Res. 1988; 29:469-479 [Abstract]
• Cohn J. S., McNamara J. R., Krasinski S. D., Russell R. M., Schaefer E. J. Role of triglyceride-rich lipoproteins from the liver and intestine in the etiology of postprandial peaks in plasma triglyceride concentration. Metabolism 1989; 38:484-490 [Medline]
• Davidson M. H., Kong J. C., Drennan K. B., Story K., Anderson G. H. Efficacy of the National Cholesterol Education Program Step I Diet. A randomized trial incorporating quick-service foods. Arch. Intern Med. 1996; 156:305-312
• Ebenbichler C. F., Kirchmair R., Egger C., Patsch J. R. Postprandial state and atherosclerosis. Curr. Opin. Lipidol. 1995; 6:286-290 [Medline]
• Fiore M. D., Mitchell J., Doan T., Nelson R., Winter G., Grandone C., Zeng K., Haraden R., Smith J., Harris K., Leszczynski J., Berry D., Safford S., Barnes G., Scholnick A., Ludington K. The Abbott IMx automated benchtop immunochemistry analyzer system. Clin. Chem. 1988; 34:1726-1732 ^{[Abstract/Free Full Text]}
• Friedewald W. T., Levy R. I., Fredrickson D. S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin. Chem. 1972; 18:499-502 [Abstract]
• Gianturco S. H., Bradley W. A. Lipoprotein-mediated cellular mechanisms for atherogenesis in hypertriglyceridemia. Semin. Thromb. Hemostasis 1988; 14:165-169 [Medline]
• Grundy S. M., Nix D., Whelan M. F., Franklin L. Comparison of three cholesterol-lowering diets in normolipidemic men. J. Am. Med. Assoc. 1986; 256:2351-2355 [Abstract]
• Grundy S. M., Denke M. A. Dietary influences on serum lipids and lipoproteins. J. Lipid Res. 1990; 31:1149-1172 [Abstract]
• Heller F. R., Vandenplas C., Desager J. P., Harvengt C. The vitamin A fat-loading test in young normolipidemic subjects. Clin. Chim. Acta. 1993; 219:167-176 [Medline]
• Hollenbeck C. B., Coulston A. M. Effects of dietary carbohydrate and fat intake on glucose and lipoprotein metabolism in individuals with diabetes mellitus. Diabetes Care 1991; 14:774-785 [Abstract]
• Hudgins L. C., Hellerstein M., Seidman C., Neese R., Diakun J., Hirsch J. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J. Clin. Invest. 1996; 97:2081-2091 [Medline]
• Jackson R. L., Kashyap M. L., Barnhart R. L., Allen C., Hogg E., Glueck C. J. Influence of polyunsaturated and saturated fats on plasma lipids and lipoproteins in man. Am. J. Clin. Nutr. 1984; 39:589-597 [Abstract/Free Full Text]
• Lewis G. F., O'Meara N. M., Soltys P. A., Blackman J. D., Iverius P. H., Pugh W. L., Getz G. S., Polonsky K. S. Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities. J. Clin. Endocrinol. Metab. 1991; 72:934-944 [Abstract]
• Lichtenstein A. H., Ausman L. M., Carrasco W., Jenner J. L., Ordovas J. M., Schaefer E. J. Short-term consumption of a low-fat diet beneficially affects plasma lipid concentrations only when accompanied by weight loss. Hypercholesterolemia, low-fat diet and plasma lipids. Arterioscler. Thromb. 1994; 14:1751-1760 [Abstract/Free Full Text]
• Myers G. L., Cooper G. R., Winn C. L., Smith S. J. The Centers for Disease Control-National Heart, Lung, and Blood Institute Lipid Standardization Program. An approach to accurate and precise lipid measurements. Clin. Lab. Med. 1989; 9:105-135
• National Cholesterol Education Program (1993) Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. U.S. Department of Health and Human Services Publication No. NIH 93-3095.
• Neese J. W. Glucose, direct hexokinase method. Selected methods. Clin. Chem. 1982; 9:241-248
• Nestel P. J. Relationship between plasma triglycerides and removal of chylomicrons. J. Clin. Invest. 1964; 43:943-949
• Ooi T. C., Simo I. E., Yakichuk J. A. Delayed clearance of postprandial chylomicrons and their remnants in the hypoalphalipoproteinemia and mild hypertriglyceridemia syndrome. Arterioscler. Thromb. 1992; 12:1184-1190 [Abstract]
• Patsch J. R., Miesenbock G., Hopferwieser T., Muhlberger V., Knapp E., Dunn J. K., Gotto A. M., Patsch W. Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state. Arterioscler. Thromb. 1992; 12:1336-1345
• Sampugna, J. Pallansch, L. A., Enig M. G., Keeney M. Rapid analysis of trans fatty acids on SP2340 glass capillary columns. J. Chromatogr. 1982; 249:245-255
• Shepherd, J., Packard, C. J., Patsch, J. R., Gotto, A. M. & Taunton, O. D. (1982) Effects of dietary polyunsaturated and saturated fat on the properties of high density lipoproteins and the metabolism of apolipoprotein A-I. J. Clin. Invest. 1582-1592.
• Walden, C. E., Retzlaff, B. M., Buck, B. L., McCann, B. S. & Knopp, R. H. (1997) Lipoprotein lipid response to the National Cholesterol Education Program Step II diet by hypercholesterolemic and combined hyperlipidemic women and men. Arterioscler. Thromb. Vasc. Biol. 375-382.
• Wardlaw G. M., Snook J. T. Effect of diets high in butter, corn oil, or high-oleic acid sunflower oil on serum lipids and apolipoproteins in men. Am. J. Clin. Nutr. 1990; 51:815-821 [Abstract/Free Full Text]
• Warnick G. R., Albers J. J. A comprehensive evaluation of the heparin-manganese precipitation procedure for estimating high density lipoprotein cholesterol. J. Lipid Res. 1978; 19:65-76 [Abstract]
• Winer, B. J. (1971) Statistical Principles in Experimental Design, 2nd ed. pp 514-603. McGraw-Hill Book, New York.
• Weisweiler P., Janetschek P., Schwandt P. Influence of polyunsaturated fats and fat restriction on serum lipoproteins in humans. Metabolism 1985; 34:83-87 [Medline]
• Zilversmit D. B. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin. Chem. 1995; 41:153-158 [Abstract/Free Full Text]

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