Asia Pacific J Clin Nutr (1997) 6(1): 26-30

Dietary oleic and palmitic acid exert similar effects on plasma lipids and lipoprotein metabolism in hamsters fed purified diets with low cholesterol but different quantities of fat

Pramod Khosla PhD, Andrzej Pronczuk DSc, Tahar Hajri PhD and
KC Hayes DVM, PhD
Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA, USA

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The current study was designed to determine whether the transition from a low-fat (20% en) to a high-fat (40% en) diet through incremental increases in specific fatty acids (16:0 or 18:1) would exert a differential effect on plasma lipids and lipoprotein metabolism. Male Golden Syrian hamsters were fed purified diets in which the dietary fat (fatty acids) content was varied by blending different dietary oils. Animals were fed one of 5 purified diets: a low-fat control diet with 20% en fat; two diets with 30%en from fat; and two diets with 40% en from fat. In each case the extra fat was supplied either by oleic acid or palmitic acid. Dietary myristic (0 - 0.50% en) and linoleic acid (5.2 -5.9% en) were relatively constant across all diets, which contained a low level of cholesterol (~40 mg/1000 kcal). Diets were formulated so that protein, vitamins and minerals were constant per calorie. All animals were fed a fixed amount of calories for 6-8 week periods. Plasma lipids (n=15-20 per group) and lipoprotein cholesterol concentrations were determined following sequential ultracentrifugation, from individual animals (n=5-6 per group). Increasing dietary fat from 20% en to 30% en to 40% en, by increasing oleic acid (6.9% en to 16.5% en to 24.8% en respectively), did not affect total cholesterol (TC), triglyceride (TG) or lipoprotein cholesterol concentrations. Similarly, increasing dietary fat from 20% en to 30% en to 40% en, by increasing palmitic acid (6.6% en to 12.9% en to 21 % en) had no affect on plasma lipids or lipoprotein cholesterol. The similarity in plasma and lipoprotein cholesterol levels was further confirmed by kinetic studies (at 8 weeks) in which animals were injected simultaneously with either radiolabeled native LDL and methylated LDL or radiolabeled native LDL and HDL. Consistent with the similarities in circulating LDL-C concentrations, there was no difference in the clearance (ie fractional catabolic rates and half-lives) of LDL by either receptor-mediated or receptor-independent pathways. Similarly, in agreement with the similar HDL-C concentrations, no difference was observed in HDL fractional catabolic rates. Thus, if dietary myristic acid is low and linoleic acid is adequate and constant, dietary 16:0 and 18:1 can be readily interchanged, across a wide range of energies without compromising the plasma lipid profile in normocholesterolaemic animals consuming low-cholesterol diets. Whether this 16:0/18:1 equivalence is dependent on the relatively low levels of dietary cholesterol and/or adequate amounts of linoleic acid (~5 to 6% en) remains to be established.

Key words: Dietary fat, oleic acid, palmitic acid, lipoprotein, LDL receptor activity

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Introduction
Current dietary guidelines advocate reductions in total fat consumption, saturated fatty acid and dietary cholesterol intake, as a primary means for lowering low density lipoprotein cholesterol concentrations (LDL-C), and thereby reducing subsequent risk from coronary heart disease (CHD). While there is much data on the effects of specific fatty acids on plasma lipids, the role of these individual fatty acids within the context of the total fat load is relatively unexplored. Most studies which have assessed fat quantity in modulating plasma lipids, have utilised, at least in experimental animals, the same basic fat fed at different levels in the diet^1,2. However, a distinct disadvantage in these types of studies is that while total fat quantity and specific fatty acid content changes, the relative mix or proportion of the various fatty acids remains unaltered. Thus feeding a specific fat at 40% en and subsequently at 30% en, results in decreased consumption of all the fatty acids present in the parent fat, but the relative mix of fatty acids in the parent fat is maintained at both fat loads. Hence the results maintained may reflect decreased total fat consumption or decreases in one or more fatty acids.

The current study was undertaken to explore what effect the mix of fatty acids has when fat quantity alters. Previously, using cholesterol-free purified diets fed to non human primates, or gerbils and hamsters, the results of several studies from this laboratory have revealed that under these conditions, myristic acid (14:0) and linoleic acid (18:2) are key determinants of plasma lipids^3-11. When LDL receptors are down-regulated (either by feeding excessive dietary cholesterol or for genetic reasons), palmitic acid (16:0) becomes a major determinant of the resulting lipid response. These studies have suggested that if the levels of 14:0 and 18:2 are controlled in situations in which LDL receptor activity is not compromised, 16:0 and oleic acid (18:1) can be readily interchanged without impacting plasma lipids. The results of recent human studies are in support of this tenet^12-15, but only when total fat intake is ~30% en. This interchange does not appear, based on regression analyses^9,10, to depend on the total fat load. However the above mentioned studies from this laboratory were carried out at only one fat level (30% en in non-human primates and 40% en in hamsters and gerbils). Thus to test the applicability of these findings to situations of multiple fat levels (eg 20% en, 30% en and 40% en) the current study was conducted in hamsters. The hypothesis tested was that using low levels of dietary cholesterol, fat quantity could be altered - specifically by manipulating 16:0 and 18:1, without affecting plasma lipids or lipoprotein metabolism provided 14:0 and 18:2 levels were unchanged. To test this objective, hamsters were fed different purified diets in which dietary fat quantity was varied (from 20% en ->30% en ->40% en) by blending different dietary oils such that the increase in fat reflected increases in either 16:0 or 18:1. Most importantly, the blends were prepared such that regardless of the fat quantity, 14:0 levels (0-0.5% en) and 18:2 levels (5.2-5.9% en) were essentially constant across diets.

Materials and Methods
Animals, diets and study design. 101 male hamsters (Lakeview strain: age ~6 months) were obtained from Charles River Laboratories. They were housed 3-4 animals per cage and fed laboratory chow (ad libitum) for 5 weeks. At this time, fasting plasma cholesterol and triglyceride concentrations were determined in a random subset of 33 animals. All animals were then switched to a cholesterol-free low-fat purified diet (run-in diet) with 20% en from fat, and provided with a fixed amount of diet per day (~52 kcal/animal/ day). After 2 weeks of feeding this diet, fasting plasma cholesterol and triglyceride concentrations were determined in another random subset of 33 animals. Animals were then randomly divided into 5 groups and each group was assigned to one of 5 different purified diets (Table 1).

Table 1. Composition of hamster purified diets (g/100 g)^a

Ingredient	Diet lb	Diet 2	Diet 3	Diet 4	Diet 5
Casein	22.2	23.7	25.35	23.7	25.35
Cornstarch	34.75	25.9	16.15	25.9	16.15
Glucose	13.3	14.2	15.2	14.2	15.2
Cellulose	15.0	16.0	17.15	16.0	17.15
Fat: (Total)	8.25	13.25	18.75	13.25	18.75
Palm Oil	5.25	3.6	3.75	8.68	1.88
Olive Oil-1 (7% 18:2)	-	-	3.75	-	-
Olive Oil-2 (15% 18:2)	0.9	8.7	13.13	-	-
Palm Stearin	-	-	-	2.65	14.53
Safflower Oil	2.1	0.95	-	1.93	2.35
Mineral mixc	5.0	5.34	5.71	5.34	5.71
Vitamin mixd	1.2	1.28	1.37	1.28	1.37
Choline Cl2	0.3	0.32	0.34	0.32	0.34
Cholesterole	0.015	0.016	0.017	0.016	0.017

(a) Diets were prepared in 2 kg batches by adding 120g of cornstarch to 1600mL water to make a gel. Then the remainder of the diet was mixed in as the gel set. (b) Diet codes; 1 - low fat control diet; 2 - medium fat oleic acid-rich diet; 3 - high fat oleic acid-rich diet; 4 - medium fat palmitic acid-rich diet and 5 - high fat palmitic acid-rich diet. (c) Ausman-Hayes mineral mix. (d) Hayes-Cathcart vitamin mix. (e) cholesterol was dissolved in the hot oils prior to mixing with the remaining dietary ingredients.

The control diet (Diet 1) was relatively low in fat (20% en). Diet 2 was a medium-fat oleic acid enriched diet with 30% en fat. Diet 3 was a high-fat oleic acid-enriched diet with 40% en fat. Diet 4 was a medium-fat palmitic acid-enriched diet with 30% en from fat. Diet 5 was a high-fat palmitic acid-enriched diet with 40% en from fat. All 5 diets also contained cholesterol at 40mg/1000 kcal of diet. Diets were formulated with different blends of fats such that in addition to varying the total fat load (at the expense of carbohydrate), specific fatty acids were also varied. Thus relative to Diet 1, the extra fat in Diets 2 and 3 was specifically oleic acid, whereas the extra fat in Diets 4 and 5 (again c.f. Diet 1), was provided specifically by palmitic acid. Dietary myristic acid (14:0) and linoleic acid (18:2) was relatively uniform across all 5 diets -0 to 0.50% en and 5.2 to 5.9% en, respectively. Diets were formulated with the same nutrient densities (Table 2), and the fatty acid composition of the diet (Table 3) as fed was verified by GLC⁵. Irrespective of the dietary fat load, animals continued to receive a fixed amount of calories (~52 kcal/animal/ day). Hence the design of the study allowed for the evaluation of the effects of increasing the dietary fat load, when only one fatty acid increases. Animals were fed their respective diets for up to 8 weeks during which time plasma and lipoprotein lipids as well as in vivo lipoprotein metabolism were evaluated as detailed in subsequent sections. All procedures and protocols were in accordance with the University’s Animal Use and Radiation Safety Committees.

Plasma and lipoprotein lipid determinations. Individual hamsters were fasted overnight (~16 hours) in hanging cages. Blood was collected by cardiac puncture (following light anaesthesia with 50% O₂/50% CO₂) using an EDTA-wetted syringe, and transferred to EDTA-containing tubes which were kept on ice. Plasma was isolated by centrifugation at 1000x g, 10 min, 4°C. Lipoprotein fractions were isolated either by discontinuous density gradient or sequential ultracentrifugation as indicated in the text. Cholesterol and triglyceride concentrations in both plasma and lipoprotein fractions were determined enzymatically (kit #352 and #336 respectively, Sigma DiagnosticsR^TM, St. Louis, MO).

Lipoprotein isolations. Prior to isolation of any lipoprotein, sodium azide, gentamycin sulfate, benzamidine and EDTA were added to all plasma samples^16,17. Plasma, pooled according to diet, was utilised for separation of lipoproteins using a 5-step salt gradient by density gradient ultracentrifugation exactly as detailed by Goulinet and Chapman¹⁸. Following ultracentrifugation at 15°C, 35k for 48 hours in a SW 41.1 rotor, 30 fractions were collected (a top fraction of 500 mL, and 29 subsequent fractions of 400 mL each). The cholesterol content of each fraction was determined enzymatically, as well as the density of each fraction as described elsewhere¹¹. Based on the above cholesterol and density distributions, subsequent lipoprotein isolations utilised a Ti 50.4 fixed angle rotor to isolate VLDL+IDL (d<1.02 g/mL), LDL (1.02<d<1.05 g/mL) and HDL (1.05<d<l.18 g/mL) by sequential ultracentri-fugation¹⁹. In the rest of this report the VLDL+IDL fraction will be referred to simply as VLDL.

Table 2. Caloric content of hamster diets (kcal/ l00g diet)

Ingredient	Diet 1	Diet 2, 4	Diet 3, 5
Casein	88.8 (24%en)	94.8 (24.3%en)	101.4 (24.6%en)
Cornstarch	139 (38%en)	103.6 (27%en)	64.6 (16%en)
Glucose	53.2 (14%en)	56.8 (15%en)	60.8 (15%en)
Cellulose	15 (4%en)	16 (4%en)	17.1 (4%en)
Fat	74.25 (20%en)	119.25 (31%en)	168.75 (41%en)
Total	370	390	413
Cholesterola	40.5	40.5	40.5
Mineralsb	13.5	13.7	13.8
Vitaminsb	3.24	3.28	3.32

^a mg/1000 Kcal; ^bg/1000 Kcal

Table 3. Fatty acid composition of hamster purified diets (%energy).

Fatty acid	Diet 1	Diet 2	Diet 3	Diet 4	Diet 5
14:0	0.4	0	0.1	0.3	0.5
16:0	6.6	6.7	7.7	12.9	21.9
18:1	6.9	16.5	24.8	9.5	9.9
18:2	5.2	5.9	5.4	5.6	5.9

Diets were analysed by GLC.

Preparation of lipoprotein tracers. Six days prior to commencement of the turnover study, several hamsters from each group were fasted individually for 16h in hanging cages. Following anaesthesia with 50%O₂/50%CO₂, they were exsanguinated by cardiac puncture. Plasma was harvested following centrifugation, and LDL (1.02 < d < 1.05 g/mL) and HDL (1.05 < d < 1. 18 g/mL) were isolated from pooled plasma by sequential ultracentrifugation and washed and concentrated by recentrifugation at their appropriate densities. Following dialysis (0.15 M NaCl/ lmM EDTA pH 7.4), lipoprotein protein concentration was determined using Markwell’s modification²⁰ of the Lowry procedure²¹. The LDL was divided into two aliquots, which were radiolabeled with Na¹²⁵ I and Na¹³¹I (Amersham, Chicago, IL) respectively. The ¹³¹I-LDL was subsequently reductively methylated as detailed previously⁷. Additionally, an aliquot of HDL was radiolabeled with Na¹³¹I. All three tracers were extensively dialyzed against saline prior to injection. For all three tracers the intramolecular distribution of radioactivity was determined⁷. For both the native ¹²⁵I-LDL and methylated ¹³¹I-LDL, apo B associated radioactivity was ~88%, while for ¹³¹I-HDL, protein-bound radioactivity was in excess of 97%.

Protocol for metabolic studies. Potassium iodide (0.1 g /l00mL) was added to the drinking water of all hamsters 48 hours before injection of tracers. Hamsters were injected simultaneously with either ¹²⁵I-LDL and methylated ^l3lI-LDL or ^l251-LDL and ¹³¹I-HDL via the jugular vein. A 100 mL blood sample was obtained by cardiac puncture at 2 min post-injection. Subsequent blood samples (100mL) were obtained periodically by cardiac puncture over the next 48 hours. At each instance the hamsters were lightly anaesthetised with 50%O₂/50%CO₂. All animals continued to have access to KI-supplemented water until 2 days after collection of the last blood sample. All blood samples were kept on ice until the separation of plasma. Duplicate aliquots of plasma (20-50 mL) were counted for determination of ¹²⁵I- and ¹³¹I-associated radio activities.

Kinetic analyses Plasma ¹²⁵I- and ¹³¹I radioactivity data were bi-exponential for all three tracers, and were therefore analysed in accordance with a 2-pool model²² and their half-lives and fractional catabolic rates (FCR) were calculated²³. The assumptions and rationale for using the 2-pool model have been detailed previously^7,8. Additionally, the limitations of the analyses in using HDL concentrations and the FCR for whole HDL, as a measure of HDL apo A1 metabolism have been discussed⁸.

Statistical Analyses All statistical analyses were performed using a Power Macintosh 6100R ^TM computer (Apple Systems Inc., Cupertino, CA) with the Statview 512+^TM (Brain Power Inc., Calabasca, CA) statistical package. Significant differences were calculated using a one way analysis of variance test. Results are presented as the mean±SD.

Results
Body weights, plasma cholesterol and triglyceride concentrations averaged 157 ± 17 g, 149 ± 16 mg/dL and 136 ± 40 mg/dL, respectively (mean ± SD, n=33) in the hamsters at the end of the 2-week run-in period.Body weights and plasma lipids after 6 weeks of feeding the test diets are shown in Table 4. There were no significant dietary effects on any of the measured parameters. The 6 week data was not significantly different from the 4 week data (results not shown), indicating that the animals had achieved a steady-state with respect to their plasma lipid concentrations. In accordance with the plasma lipid data, there were no discernible differences in the lipoprotein cholesterol concentrations measured after sequential ultracentrifugation of plasma from individual animals (Table 5). For all diets, VLDL-C averaged ~13% of total lipoprotein cholesterol, while the figures for LDL and HDL were ~21% and ~66%, respectively.

The 6 week lipoprotein isolations were carried out by sequential ultracentrifugation and VLDL, LDL and HDL were isolated at the density intervals d<1.02g/mL, 1.02<d<1.05 g/mL and 1.05<d<l.18 g/mL, respectively. These density cuts were based on the 4 week lipoprotein isolations carried out by discontinuous density gradient ultracentrifugation (Figure 1) which also revealed no diet effects.

Clearance of native LDL, methylated LDL and HDL was assessed in a subset of 33 animals after ~8 weeks on diet, and the resulting data is shown in Table 6. Consistent with the plasma lipid data, there were no dietary influences on the FCR of native LDL, methylated LDL or HDL. Receptor-independent clearance represented ~48% of total clearance and thus receptor-dependent clearance accounted for ~52% of the total clearance. The half-life of the methylated LDL (irrespective of diet) was significantly longer than the half-life of the native LDL (21.7 ± 3.6 hrs vs.13.4 ± l.7 hrs, p = 0.0001), indicative of its longer residence time in the plasma. The half-life of whole HDL (25.4 ± 3.5 hrs) was significantly longer than the half-life for both the methylated and native LDL.

Table 4. Body weights and plasma lipid concentrations after 6 weeks.

Diet	BW (g)	TC (mg/dL)	TG (mg/dL)
#1 (18)	166±20	141±21	125±28
#2 (15)	174±13	145±16	138±26
#3 (20)	180±15	142±21	126±25
#4 (13)	169±20	151±27	147±40
#5 (14)	176±20	130±17	120±28

Values are the mean ± SD of the number of animals given in parentheses. There was no significant difference between dietary groups for any of the three parameters (assessed by ANOVA).

Table 5. Plasma and lipoprotein cholesterol concentrations (mg/dL).

Diet	TC	VLDL	LDL	HDL
#1	137±13	17±4 (13%±2%)	33±4 (24%±3%)	87±11 (63%±2%)
#2	131±16	17±4 (13%±2%)	28±5 (21%±2%)	86±7 (66%±3%)
#3	137±8	20±6 (14%±5%)	27±3 (20%±2%)	90±7 (66%±5%)
#4	139±30	19±8 (13%±3%)	29±7 (21%±4%)	91±18 (66%±4%)
#5	133±30	18±13 (13%±6%)	31±11 (23%±3%)	84±7 (64%±8%)

Lipoproteins were isolated by sequential ultracentrifugation from the plasma of individual hamsters at the following density intervals - VLDL d<1.02 g/mL; LDL 1.02<d<1.05 g/mL and HDL 1.05<d<1.18 g/m L.
Values are the mean ± SD for 5-6 hamsters per dietary group. Percentage of total lipoprotein cholesterol in parenthesis.

Discussion
The current study was conducted in order to evaluate the effects of increasing dietary fat quantity - specifically by increasing only one fatty acid - on plasma lipids. Theoretically, the study might have started with a control diet of 40% en (with equivalent contributions from SFA, MUFA and PUFA) in which fat quantity decreased to 30% en and 20% en by decreasing either 16:0 or 18:1. However, this design was not possible given the limitation that we wished to utilise naturally occurring oils, as opposed to artificially generated triglycerides, on the assumption that triglyceride structure may affect lipoprotein metabolism. Thus a 20% control diet was selected in which SFA, MUFA and PUFA were roughly in a 1/1/1 ratio. With this control diet as a starting point, it was possible to formulate diets with 30% en or 40% en from fat, in which the excess fat was contributed by either 18:1 or 16:0, but, 14:0 and 18:2 were held constant. Within this design frame, the results clearly show that within a 20% en to 40% en dietary fat load, 16:0 and 18:1 can be readily interchanged without having any effect on plasma total or lipoprotein cholesterol concentrations. This was further reflected in the in vivo kinetic data, which revealed no dietary effects on LDL and HDL clearance rates.

Figure 1. Cholesterol and density distribution of plasma lipoproteins isolated by discontinuous density gradient ultracentrifugation (DDGUC).

Lipoproteins were isolated by DDGUC and 30 fractions collected. The cholesterol content of each fraction as well as its density was determined. Profile shown is from the control diet (Diet 1). Similar results were obtained with the plasma from the other diets.

Table 6. Clearance of native LDL, methylated LDL and HDL.

Diet		nat LDL			meth LDL			HDL
		FCR pools/day	t 1/2 hrs		FCR pools/day	t 1/2 hrs		FCR pools/day	t 1/2 hrs
#1	(7)a	1.805+0.297	14.30±1.81	(3)	0.89±0.12	22.8±2.0	(4)	0.74±0.09	28.3±0.7
# 2	(5)	1.960±0.518	13.81±1.76	(2)	0.76,0.84	23.5,23.1	(3)	0.89±0.07	27.7±6.5
#3	(7)	2.080±0.672	13.50±1.30	(3)	0.86±0.33	23.7±6.6	(4)	0.95±0.10	23.4±2.0
#4	(6)	1.833±0.317	13.63±1.64	(3)	1.02±0.35	20.0±1.9	(3)	0.79+0.12	25.0±2.7
#5	(7)	2.542±0.898	12.04±1.35	(3)	1.24±0.21	19.6±2.4	(4)	1.08±0.30	23.1±1.9
All	(32)	2.056±0.625	13.43±1.67	(14)	0.99±0.27	21.7±3.6	(18)	0.89±0.19	25.4±3.5

^a Number of animals. A total of 33 animals were injected with ¹²⁵I-LDL, and either methylated ¹³¹I-LDL (n=15) or ¹³¹I-HDL (n=18). One animal from Diet 2 (injected with native and methylated LDL) died during the course of the turnover. Thus complete data were available from 32 animals. Values are presented as mean±SD, except for the diet 2 animals injected with methylated LDL, for whom individual values are listed. FCR’s and half-lives were calculated as indicated in the text. One way ANOVA indicated no significant difference between diets for any of the measured parameters. For all animals combined, the half life for the native LDL was significantly lower than the half-life of the methylated LDL and HDL (p=0.0001). Additionally, the half-life of the methylated LDL was significantly lower than the HDL half life (p=0.0001).

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In previous studies in hamsters² and guinea pigs^1,24, the effects of decreasing dietary fat quantity on plasma lipids were dependent largely on the basal fat employed. In the hamster, plasma LDL decreased when the basal fat was principally hydrogenated coconut oil (HCO) and fat quantity was decreased from 40% en to 20% en². While the above effect was attributed to the SFA content of the diet, the current data suggests that altered intake of 14:0 and 18:2 may have been responsible, especially as HCO a) has a very high 14:0 content and b) no 18:2. Although safflower oil was blended into the HCO-based diet, the levels of 18:2 were considerably less than the ~5% en employed in the current study. Similarly, in the guinea pig studies, varying fat quantity between 19% en and 35% en modulated plasma lipids differentially depending on whether the basal fat was lard, olive oil or corn oil. However, in each of these fats the levels of 14:0 or 18:2 were not constant.

The current study which evaluated 16:0 and 18:1 exchanges revealed no effects on plasma lipids even though diets provided cholesterol (albeit at low levels). However, the "lack" of cholesterol was not the factor in determining the response. The hamster when fed a cholesterol-free purified diet based solely on coconut oil (high 14:0, low 18:2) exhibits a plasma cholesterol almost 60-70 mg/dL higher than the levels observed when safflower oil (no 14:0, high 18:2) is the dietary fat source (Pronczuk et al, unpublished). This differential response is magnified in the gerbil (almost 120 mg/dL), but a similar study employing the same diets (devoid of cholesterol) also revealed that increasing fat quantity from 20% en to 30% en to 40% en had no effect on plasma lipids when the excess fat was 16:0 or 18:1. However, plasma lipids increased when the excess fat was from 14:0 and decreased when the excess fat was from 18:2 (Khosla et al, unpublished).

Thus the results of the current study lend support to the previous observations from this laboratory^7,10,25 that in situations of normal LDL receptor activity, 16:0 and 18:1 can be readily interchanged without compromising plasma lipids provided 14:0 levels are tightly controlled and 18:2 levels are adequate.

While the current design may be difficult to test using Western type diets in humans, the results may be of relevance to populations accustomed to low levels of fat intake. In India and China, dietary fat constitutes ~15% en. With increasing economic prosperity, fat intake is on the increase in certain sections of the population. The current data, cautiously extrapolated to humans, would suggest that if fat consumption increases, it would be prudent to balance the intakes of 14:0 and 18:2 as fatty acids increase.

Acknowledgment. This study was funded partially by Palm Oil Research Institute of Malaysia (PORIM).

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Dietary oleic and palmitic acid exert similar effects on plasma lipids and lipoprotein metabolism

in hamsters fed purified diets with low cholesterol but different quantities of fat
Pramod Khosla, Andrzej Pronczuk, Tahar Hajri and KC Hayes
Asia Pacific Journal of Clinical Nutrition (1997) Volume 6, Number 1: 26-30

Copyright © 1993 [Asia Pacific Journal of Clinical Nutrition]. All rights reserved.
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