Journal of Nutrition OpenSOurce Diets- www.ResearchDiets.com

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Khosla, P.
Right arrow Articles by Hayes, K. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khosla, P.
Right arrow Articles by Hayes, K. C.

The Journal of Nutrition Vol. 127 No. 3 March 1997, pp. 525S-530S
Copyright ©1997 by the American Society for Nutritional Sciences

Decreasing Dietary Lauric and Myristic Acids Improves Plasma Lipids More Favorably Than Decreasing Dietary Palmitic Acid in Rhesus Monkeys Fed AHA Step 1 Type Diets1,2,3,4

Pramod Khosla5, Tahar Hajri, Andrzej Pronczuk, and K. C. Hayes6

Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA, 02254

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
FOOTNOTES
LITERATURE CITED

ABSTRACT

Current dietary recommendations advocate reductions in saturated fatty acids (SFA) and cholesterol (C) as a primary intervention for achieving a more desirable plasma lipid profile. To ascertain whether it is more efficacious to decrease dietary lauric and myristic acids (12:0 + 14:0) or dietary palmitic acid (16:0) in conjunction with a reduction in dietary C, 11 rhesus monkeys (8 males, 3 females) were initially fed a control diet rich in SFA + C for 14 wk [dietary fat ~38% of energy (%en), SFA 16%en and C at 180 mg/1000 kcal]. Plasma lipids were measured between the 9th and 13th wk, and LDL metabolism was assessed after 13 wk. Monkeys were then split into two groups and fed one of two American Heart Association (AHA) Step 1 diets (~30%en fat, 10%en SFA, 75 mg cholesterol/1000 kcal) for an additional 14 wk, and plasma lipids and LDL metabolism were re-evaluated. Group 1 received a 16:0-rich diet in which most 12:0 + 14:0 were deleted (~8.6%en from 16:0 and ~0.3%en from 12:0 + 14:0), whereas Group 2 received a diet rich in 12:0 + 14:0 from which 16:0 was selectively removed (2.6%en from 16:0 and ~6.3%en 12:0 + 14:0). In all three diets, oleic and linoleic acid were held relatively constant so that only SFA, the level of total fat and cholesterol were manipulated. Only the Step 1 diet that selectively removed 12:0 + 14:0 (the 16:0-rich diet) significantly reduced all lipid fractions, including total cholesterol (TC), HDL-C, LDL-C, apolipoprotein B (apoB) and the LDL pool size. Plasma triglyceride (TG) and the ratio of TC/HDL-C were not altered by either Step I diet. The smaller LDL pool size following the 16:0-rich diet in Group 1 was attributable to a significantly higher fractional catabolic rate (FCR) of LDL because the transport rate of LDL apoB was unaffected. Although the FCR was increased with the 12:0 + 14:0-rich diet, the LDL apoB pool was not affected because the transport rate of LDL tended to increase as well. The data suggest that a Step 1 diet that reduces total fat by decreasing 12:0 + 14:0 in conjunction with dietary C, improves plasma lipids more favorably than a similar diet that selectively removes 16:0 and C. Previous data would imply that the benefit resulted from removal of 12:0 + 14:0 per se, but the possibility is not eliminated that removal of C (independent of 12:0 + 14:0) muted the potential interaction between C and palmitic acid that tends to raise TC.

Key words: palmitic acid, lauric and myristic acids, rhesus monkeys, fatty acids, LDL kinetics, plasma cholesterol.

INTRODUCTION

Reducing dietary saturated fatty acids (SFA)7 and cholesterol as a primary means of achieving a more desirable plasma lipid profile [and consequently decreasing the risk of coronary heart disease (CHD)] has been advocated by various health agencies (National Research Council 1992, Surgeon General's Report 1988, The Expert Panel 1988 and 1993). The rationale for this recommendation lies in the observation that SFA raise total cholesterol (TC) [especially low density lipoprotein cholesterol (LDL-C)], whereas polyunsaturated fatty acids (PUFA) lower it, and monounsaturated fatty acids (MUFA) are neutral (Hegsted et al. 1965, Keys et al. 1965).

Recent data, however, from both humans and animal models, suggest that even among lauric, myristic and palmitic acids, their relative "hypercholesterolemic effects" are not similar when fed as natural triglycerides (Hayes and Khosla 1992, Mensink and Katan 1992, Sundram et al. 1994, Yu et al. 1995). For example, palmitic acid (16:0) has been demonstrated to be as "neutral" as oleic acid (18:1) under metabolic conditions in which lipoprotein metabolism is unstressed and dietary cholesterol intake is low (Choudhury et al. 1995, Hayes and Khosla 1992, Ng et al. 1992, Sundram et al. 1995, Vergroesen and Gottenbos 1975). Because it is possible to utilize a variety of dietary fats that meet the National Cholesterol Education Program/American Heart Association (NCEP/AHA) Step 1 diet recommendations in terms of the total SFA content, i.e., <= 10% of energy (%en), we evaluated the relative benefit of selectively reducing 12:0 + 14:0, as opposed to 16:0, within the context of SFA reduction when designing Step I diets.

Fatty acid analyses of the diets as fed, was performed by gas liquid chromatography as stated in the text. P/S, polyunsaturated/saturated fat.

MATERIALS AND METHODS

Animals and diets. Eleven normocholesterolemic rhesus monkeys (Macaca mulatta), aged 15-21 y, that had been fed purified diets from birth were studied. For these experiments, three different purified diets were fed (Table 1). The control diet approximated the average American diet in terms of the total fat (38%en) and dietary cholesterol content (180 mg/1000 kcal), whereas the two test diets were formulated according to the guidelines of the AHA for Step 1 diets, i.e., total fat and cholesterol were reduced to ~30%en and 75 mg/1000 kcal, respectively. The reduction in dietary fat was achieved at the expense of carbohydrate. Both test diets had a substantially lower content of SFA (~40% less) compared with the control diet, and modestly lower monounsaturated fatty acid (MUFA) content (~14% less) (Table 2). The two test diets provided equivalent energy from SFA, MUFA and polyunsaturated fatty acids (PUFA). To eliminate any confounding effects of the PUFA in this study, we deliberately kept their content similar across all three diets. (Accordingly, the PUFA content of the control diet was somewhat higher than typical "average American" diet.) Among the test diets, the palmitic acid-rich diet (16:0-rich diet) provided 8.6%en from 16:0 and <0.3%en from 12:0 + 14:0 (combined because they always occur together in natural triglycerides). The lauric/myristic acid-rich diet (12:0 + 14:0-rich diet) supplied 2.6%en from 16:0 and 6.4%en from 12:0 + 14:0. Thus, the two test diets allowed for a comparison of a ~6%en exchange between 16:0 and 12:0 + 14:0 while meeting the requirement for SFA reduction of Step I diets. Fatty acid analyses of the diets, as fed, were verified by gas liquid chromatography (GLC), as detailed previously (Pronczuk et al. 1991).

Table 1. Composition of purified diets

[View Table]

Table 2. Percentage of total dietary calories contributed by each fatty acid

[View Table]

Study design. A parallel study design was employed. All monkeys were initially fed the control diet for 14 wk, during which time plasma lipids were sampled three times (twice during the 9th week, on consecutive days and once after 13 wk). LDL metabolism was assessed after 13 wk. Subsequently, monkeys were divided into two groups of six and five to balance their total plasma cholesterol and HDL cholesterol (HDL-C) concentrations. Group 1 was assigned to the 16:0-rich diet, and Group 2 to the 12:0+14:0-rich diet Diets were again fed for 14 wk, and lipids and LDL metabolism re-evaluated at the times indicated for the control period. As in previous studies (Hayes et al. 1991, Khosla and Hayes 1992 and 1993, Pronczuk et al. 1991), each monkey was fed a fixed amount of diet each day (~120-260 g/d as a starch-gel) that ensured maintenance of a constant body weight. However, because of the different energy densities of the control and test diets, each animal received a fixed amount of total calories during the entire study (~860 kcal/d for each monkey; range 520-1070 kcal/d). Additionally, the protein and micronutrient content of the control and test diets was adjusted such that all monkeys received a constant relative intake of nutrients during all phases of the study. The mean caloric intake for the Group 1 monkeys averaged 876 ± 158 kcal/d during the control and test periods, whereas the intake was 847 ± 204 kcal/d for the Group 2 monkeys. All procedures and protocols were in accordance with the University's Animal Use and Radiation Safety Committees.

Plasma lipid determinations. Following an overnight fast (14-16 h), monkeys were anesthetized with an intramuscular injection of Ketamine HCl (Vetalar, Parke-Davis, Morris Plains, NJ, 10 mg/100 µL) at a dose of 4-9 mg/kg body weight. Blood was obtained from the femoral vein and placed into EDTA-wetted tubes kept on ice. Plasma was isolated by centrifugation at 1000 × g, 20 min, 4oC. Total plasma cholesterol (TC) and triglyceride (TG) concentrations were determined enzymatically (kit #352 and #336, respectively, Sigma Diagnostics, St. Louis, MO). HDL-C concentrations were determined in the supernatant of plasma samples following precipitation with phosphotungstic acid/Mg2+ (HDL cholesterol reagent, #352-4, Sigma Diagnostics). The difference between TC and HDL cholesterol represented non-HDL cholesterol (i.e., VLDL + LDL cholesterol).

Preparation of lipoprotein tracers. Six days prior to commencement of a turnover study, the monkeys were deprived of food for 16 h; following sedation with ketamine, 12-15 mL blood was withdrawn from the femoral vein of each animal into EDTA-wetted tubes using a 22- gauge needle. Plasma was harvested, and sodium azide, gentamycin sulfate, benzamidine and EDTA were added (Edelstein and Scanu 1986, Schumaker and Puppione 1986). LDL (1.019 < d < 1.063 g/mL) was isolated from plasma (pooled according to diet) by sequential ultracentrifugation (Havel et al. 1955) as detailed previously (Khosla and Hayes 1992). The isolated LDL was washed and concentrated by recentrifugation at its appropriate density. Following dialysis (0.15 mol/L NaCl:1 mmol/L EDTA pH 7.4), lipoprotein protein concentration was determined using Markwell's modification (Markwell et al. 1978) of the Lowry procedure (Lowry et al. 1951). LDL was radiolabeled with Na131I or Na125I (Amersham, Chicago, IL) (to specific activities of ~300 cpm/ng), and the intramolecular distribution of radioactivity was determined (Khosla and Hayes 1992). The proportion of total radioactivity associated with apolipoprotein B (apoB) was 93 ± 2% whereas the lipid-bound radioactvity was <2%.

Table 3. Plasma lipid concentrations and LDL metabolic parameters1

[View Table]

Protocol for metabolic studies. The procedure followed previously published protocols (Khosla and Hayes 1992 and 1993). Briefly, monkeys were injected with pooled diet-homologous 125I-LDL (control diet period) or simultaneously with pooled diet-homologous 125I-LDL and pooled diet-heterologous 131I-LDL tracers (test diet period). Thus, during the test diet phase, monkeys fed the 16:0 diet were injected with diet-homologous 16:0-rich LDL as well as a trace amount of LDL prepared from animals fed the 12:0 + 14:0 diet, and vice versa. This was designed to evaluate whether host metabolic differences were more important than potential differences in particle composition (especially fatty acids). A 10-mL blood sample was collected from a femoral vein at 10 min postinjection, and additional 1-mL samples were obtained periodically up to 3 d. (The amount of blood taken from each monkey over the 3-d period averaged <7% of the estimated blood volume.) LDL was isolated by sequential ultracentrifugation from the 10-min plasma sample of each monkey (obtained following a 16-h fast), and the LDL apoB specific activity was determined (Khosla and Hayes 1992).

LDL characterization. In addition to specific activity measurements on the LDL sample (isolated from the 10-min plasma sample of the turnover study), the total cholesterol (TC) and triglyceride (TG) content was determined using enzymatic kits (see above for source). Additionally, free cholesterol (FC) and phospholipid (PL) content was determined using the Free Cholesterol C and Phospholipids B kits, respectively (Wako Pure Chemical, Osaka, Japan). Cholesteryl ester content was calculated as 1.67 × (TC - FC).

Kinetic analyses. Plasma 131I and 125I radioactivity data for both tracers were bi-exponential; the data were analyzed in accordance with a two-pool model (Matthews 1957) and the FCR calculated (Kushwaha and Hazzard 1977). The assumptions and rationale for using the two-pool model, as well as the calculations for pool sizes (mg/kg body weight) and transport rates (TR) [mg/(kg·d)] for homologous tracers, have been detailed previously (Khosla and Hayes 1992 and 1993).

Statistical analyses. All statistical analyses were performed using a Power Macintosh 6100 computer (Apple Systems, Cupertino, CA) with the Statview 512+ (Brain Power, Calabasca, CA) statistical package. Student's paired t test was used for comparison between control and test diets, whereas the unpaired t test was used for comparisons between the two test diets. Results are presented as means ± SD.

RESULTS

Prior to starting the control diet, TG, TC, HDL-C and non-HDL cholesterol concentrations for the 11 monkeys averaged 142 ± 74 mg/dL, 186 ± 30 mg/dL, 84 ± 18 mg/dL and 97 ± 22 mg/dL, respectively. The TC/HDL-C ratio was 2.25 ± 0.40. Monkeys consumed their respective diets for the duration of the study without incident. Body weights averaged 8.6 ± 1.3 kg and did not change appreciably over the course of the study.

Plasma lipid concentrations and LDL metabolic parameters. In comparison with the control diet, neither test diet affected plasma triglyceride concentrations (Table 3). Feeding the 16:0 diet (Group 1 monkeys) elicited a 15% reduction in TC (P < 0.02), a 13% reduction in HDL-C (P < 0.003) and a 16% reduction in the non-HDL cholesterol concentration (P < 0.075). Additionally, from the LDL metabolic parameters following the 16:0 diet, LDL-C was decreased by 40% (P < 0.01) and LDL apoB concentrations by 27% (P < 0.02). The 27% lower LDL apoB pool size in monkeys fed 16:0 (P < 0.02) was explained entirely by the 39% increase in fractional catabolic rate (FCR) (P < 0.0001) because the transport rate of LDL apoB was unchanged. FCR for diet-homologous and heterologous LDL tracers in 16:0-fed monkeys did not differ (1.120 ± 0.233 vs. 1.109 ± 0.193 pools/d) (Fig. 1).
Fig. 1. Decay curves depicting the decline in LDL apolipoprotein B (apoB) radioactivity. The top panel represents rhesus monkekys fed a typical American fat diet (control) and the same monkeys fed a Step 1 diet with 12:0 + 14:0 removed (i.e., the 16:0-rich fat). The bottom panel depicts the curves for monkeys fed the control diet and the Step I diet with 16:0 removed (i.e., the 12:0 + 14:0-rich fat). Diet-homologous and diet-heterologous LDL had identical decay curves for both Step 1 diets; both of the decay curves were more rapid than LDL clearance during the high fat, control period. The data suggest that the greater cholesterol intake during the control period, and not the type of saturated fatty acid, affected LDL receptor activity (clearance).
[View Larger Version of this Image (23K GIF file)]

In comparison with the control diet and in contrast to the 16:0 diet, feeding the 12:0 + 14:0 diet (Group 2 monkeys) did not significantly reduce TC or non-HDL cholesterol, whereas HDL-C was 12% lower (P < 0.02). Although the TC/HDL-C ratio was 9% higher after 12:0 + 14:0 feeding, the higher ratio did not differ significantly from the ratio obtained for the 16:0 diet. LDL-C and LDL apoB concentrations tended to decline from the control diet during 12:0 + 14:0 intake, but the decreases were not as great as those observed with the 16:0 group. The significant increase in LDL FCR in monkeys fed 12:0 + 14:0 relative to the control diet (P < 0.02) was coupled with combined tendencies (nonsignificant) for a somewhat lower LDL apoB pool size and a marginally higher transport rate of LDL apoB. As with monkeys fed the 16:0 diet, FCR for diet-homologous and heterologous LDL tracers did not differ from each other in monkeys fed the 12:0 + 14:0 diet (1.084 ± 0.272 vs. 1.088 ± 0.262 pools/d, respectively).

LDL particle characteristics. In comparison with the control diet, the LDL particles obtained from monkeys after the two test diet periods (i.e., the LDL isolated following the Step I diets) contained a slightly greater proportion of TG and >50% more PL with corresponding reductions of FC and CE, respectively (Table 4). As a result of these changes, the LDL cholesteryl ester/protein ratios were identical between the two test groups, but the ratios were 15-20% less than their respective control values. This suggests that the main effect on LDL particles was due to the reduction in dietary cholesterol and not to differences in SFA.

Table 4. LDL particle characteristics1

[View Table]

DISCUSSION

For almost three decades, reductions in dietary cholesterol and SFA intake have been advocated as a primary means for lowering LDL-C concentrations. Current guidelines recommend a SFA intake of <10% en and a cholesterol intake of <300 mg/d. These recommendations, however, do not discriminate among the different types of saturated fats and their SFA. Historically, lauric, myristic and palmitic acids have been regarded as equally cholesterol-raising (Keys et al. 1965), but a substantial body of recent data suggests that this may not be the case. Accordingly, the current study was undertaken to ascertain whether selective removal of specific SFA (either 12:0 + 14:0 or 16:0) within the context of the AHA guidelines for a Step 1 diet would have differential effects on the plasma lipid profile. Our results suggest that while decreasing either of these SFA (in conjunction with reducing dietary cholesterol) lowers LDL-C, the plasma lipid profile may improve more favorably when 12:0 + 14:0 are selectively reduced.

Both test diets in the current study provided ~10%en from SFA. However, by utilizing different blends of oils, these test diets were either rich in 12:0 + 14:0 or 16:0. The study design, therefore, allowed the evaluation of a 6%en exchange between these saturated fatty acids, while all other fatty acids (i.e., 18:0, 18:1 and 18:2) were held constant. With this subtle fatty acid manipulation, feeding of the 16:0-rich diet (i.e., the diet from which sources of 12:0 + 14:0 had been removed) elicited greater reductions in LDL levels (both cholesterol and apoB) than feeding the 12:0 + 14:0-rich diet (i.e., the diet in which 16:0 had been selectively decreased). Additionally, the 16:0-rich diet produced a smaller decline in HDL-C than the 12:0 + 14:0-rich diet Thus, although the ratio of TC/HDL-C increased slightly with the 12:0 + 14:0-rich Step 1 diet (relative to the high fat, high cholesterol control diet), this ratio was unaffected by the 16:0-rich Step 1 diet Based on the plasma lipid data alone, it is clear that feeding a Step 1 diet that selectively removed 12:0 + 14:0 was of greater benefit than feeding a Step 1 diet in which the SFA reduction was achieved by decreasing 16:0.

Review of the LDL kenetic data indicates that both test diets were equally effective in enhancing the clearance of LDL in comparison with the control diet (i.e., their FCR were higher). We would attribute this to the reduced (~60%) dietary cholesterol intake in the two Step 1 diets because dietary cholesterol has a much greater effect on LDL activity than saturated fat (Dietschy et al. 1993, Khosla and Hayes 1993). In the case of monkeys fed the 16:0-rich diet, this increase in FCR wholly accounted for the lower LDL apoB pool size because the transport rate of LDL was unaffected. In contrast, even though LDL clearance increased in monkeys fed the 12:0 + 14:0-rich diet, the pool size of LDL apoB was not reduced significantly because LDL apoB production increased. This resulted from either an increased flux of VLDL apoB to LDL apoB or from higher rates of "direct" LDL secretion, i.e., LDL derived independently of VLDL catabolism. In a previous study (Khosla and Hayes 1991), these same monkeys also exhibited a higher rate of direct LDL secretion when fed a 12:0 + 14:0-rich diet compared with the rate observed when the diet was rich in 16:0 + 18:1. Additionally, guinea pigs fed a 12:0 + 14:0-rich fat vs. a 16:0-rich fat revealed a similar disparity related to the metabolic channeling of VLDL (Abdel-Fattah et al. 1995). Although it is not possible to conclude with certainty that increased direct LDL secretion was a factor in this study (because we did not simultaneously study VLDL kinetics), it remains a likely explanation for the observed differences.

Another possibility that might contribute to the greater LDL apoB production rate observed during 12:0 + 14:0 intake would be inherent differences in the LDL particles themselves. However, both Step 1 diets resulted in circulating LDL particles having similar composition. Additionally, the FCR for diet-heterologous LDL was indistinguishable from the FCR for the diet-homologous tracer, consistent with their similar rates of clearance. Although the diet-heterologous tracer would have represented a small fraction of the endogenous LDL pool, the above observations are consistent with the interpretation that accelerated LDL clearance in monkeys fed the Step 1 diet (as opposed to the control diet) was not dependent on differences in dietary or LDL lipid fatty acid saturation and that up-regulation of hepatic LDL receptors was involved. Thus, these data further support the argument that the increased LDL receptor activity was in all likelihood attributable to the decreased cholesterol content of the Step 1 diets rather than the 6%en reduction in saturated fatty acids (Khosla and Hayes 1993).

The results from the present study suggest that the decrease in LDL-C levels induced by "decreasing SFAs" in similar human studies (e.g., Barr et al. 1992) may principally reflect a reduction in the dietary 12:0 + 14:0 content, not the 16:0 content (Hayes 1993). Evaluation of 12:0 and 14:0 by regression analysis has identified 14:0 as the primary fatty acid responsible for this effect (Hayes and Khosla 1992, Hegsted et al. 1965, Mensink and Katan 1992, Pronczuk et al. 1994). Although 14:0 typically accounts for <2%en in most conventional Western diets, it has been reported to be 4-8 times as potent as 16:0 in raising serum cholesterol, depending on the species investigated (Hayes and Khosla 1992, Hegsted et al. 1965, Mensink and Katan 1992, Pronczuk et al. 1994). Thus, a 1%en dietary reduction in 14:0 would be expected to confer at least the same benefit on TC and LDL-C as a 4%en reduction in 16:0 when cholesterol intake is minimal. However, the effects of 16:0 on TC in humans generally have been assessed with diets that also supplied a variable amount of dietary cholesterol. Based on re-evaluation of the circumstances, it appears that in situations of low cholesterol intake (<300 mg/d), 16:0 has minimal effect on plasma cholesterol (Hayes 1995, Hayes and Khosla 1992, Khosla and Sundram 1996, Pronczuk et al. 1994). The Step 1 diets used in the present study provided 75 mg cholesterol/1000 kcal (representing ~188 mg cholesterol/d for a daily caloric intake of 2500 kcal), an amount well below 300 mg/d. By the above argument, 16:0 would be predicted to have minimal if any effect on the plasma lipid profile for either of the two Step 1 diets. Accordingly, the decrease in TC and LDL-C induced by the 16:0-rich diet (compared with the control diet) is attributed to either decreased dietary cholesterol, decreased intake of 12:0 + 14:0 or both. If the hypercholesterolemic effect of 16:0 requires an interaction with dietary cholesterol (Hayes 1995, Pronczuk et al. 1994), the 16:0-rich Step 1 diet (compared with the control diet) could have precluded this interaction as a consequence of the decreased cholesterol intake.

Regardless of the above possibilities, the current study underscores the fact that the dietary 14:0 content should not be discounted simply because 14:0 represents a small increment of the dietary fatty acids. Note that for the two test diets, which provided lower intakes of saturated fat and cholesterol, replacing 6%en from 16:0 with only 1.5%en from 14:0 (+4%en from 12:0) resulted in significantly higher TC, LDL-C and LDL apoB concentrations, which in turn were not significantly different from the values observed initially when the high fat, high cholesterol control diet was fed. Although this SFA manipulation may appear subtle, our data suggest that in addition to the general recommendation to reduce all SFA, selective reduction in certain fat sources (specific SFA) should prove beneficial to the average individual. We are not aware of any human study that has evaluated this specific issue to date, but the inference from human experiments that have directly compared 12:0 + 14:0 with 16:0 (Sundram et al. 1994 and 1997) suggests that this conclusion may also apply to human subjects.

FOOTNOTES

1   Presented in a symposium at the VIIth Asian Congress of Nutrition held in Beijing, China, October 7-11, 1995. The symposium and the publication of symposium proceedings were supported in part by an educational grant from the Malaysian Palm Oil Promotion Council. Guest editor for the publication of symposium proceedings as a supplement to The Journal of Nutrition was David Kritchevsky, The Wistar Institute, Philadelphia, PA.
2   Presented in part at Experimental Biology 95, April 1995, Atlanta, GA.
3   Supported in part by a grant from the Palm Oil Research Institute of Malaysia.
4   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.
5   Current address: Department of Nutrition and Food Science, Room 3009, Science Hall, Wayne State University, Detroit, MI 48202.
6   To whom reprint requests should be addressed.
7   Abbreviations used: apoB, apolipoprotein B; C, cholesterol; CE, cholesteryl ester; CHD, coronary heart disease; %en, % of energy; FC, free cholesterol; FCR, fractional catabolic rate; GLC, gas liquid chromatography; HDL-C, HDL cholesterol; LDL-C, LDL cholesterol; MUFA, monounsaturated fatty acid; PL, phospholipid; PUFA, polyunsaturated fatty acid; SFA, saturated fatty acid; TC, total cholesterol; TG, triglycerides; TR, transport rate.

LITERATURE CITED

0022-3166/97 $3.00 ©1997 American Society for Nutritional Sciences
[Abstract/Free Full Text]



This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Khosla, P.
Right arrow Articles by Hayes, K. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khosla, P.
Right arrow Articles by Hayes, K. C.

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 1997 by American Society for Nutrition