Nutrition Research 25 (2005) 925 – 935
www.elsevier.com/locate/nutres
Effect of dietary fats on blood cholesterol and lipid and the
development of atherosclerosis in rabbits
Sun Jin Hur a, Min Dua, Kichang Nama, Mark Williamsonb, Dong Uk Ahna,T
a
Department of Animal Science, College of Agriculture, Iowa State University, Ames, IA 50011-3150, USA
b
Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames,
IA 50011-3150, USA
Received 27 August 2004; revised 29 July 2005; accepted 20 September 2005
Abstract
The objective of this study was to determine the effects of dietary fat on the development of
atherosclerosis and changes in blood lipids in rabbits. Forty New Zealand White rabbits were divided
into 5 groups and fed commercial rabbit chow with 0% oil (control), 2% corn oil, 2% fish oil, 2%
oxidized oil, or 2% heated corn oil. Cholesterol (CHO, 1.5-g/kg diet) was added to all the experimental
diets. The rabbits in the control and oxidized oil groups developed the highest scores for
atherosclerotic lesions but those fed fish oil, corn oil, and the heated corn oil groups had the lowest
lesion scores. Plasma triacylglycerol, total CHO, and low-density lipoprotein and high-density
lipoprotein CHO levels ( P b .05) in rabbits followed the trend of higher levels consistent with scores
for atherosclerotic lesions. Plasma total CHO level was one factor closely related to the development
of atherogenic lesions in the rabbit. Dietary CHO and oxidation status of dietary lipids significantly
impacted lipid metabolism and the development of atherosclerosis in rabbits. Oxidized dietary oil
accelerated the progress of atherosclerotic lesions, but polymerization of oils by heating lowered
plasma CHO level and the development of atherogenic lesions in rabbits. Heating of oil appeared to
reduce the absorption of CHO in the rabbit.
D 2005 Elsevier Inc. All rights reserved.
Keywords: Dietary cholesterol; Vegetable oil; Fish oil; Rabbit; Atherosclerosis; Plasma cholesterol
T Corresponding author. Tel.: +1 515 294 6595; fax: +1 515 294 9143.
E-mail address: duahn@iastate.edu (D.U. Ahn).
0271-5317/$ – see front matter D 2005 Elsevier Inc. All rights reserved.
doi:10.1016/j.nutres.2005.09.016
926
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
1. Introduction
The role of various dietary lipids in the control of atherosclerosis, coronary heart disease
and cancer are of considerable interest. The etiology of atherosclerosis is complex; it is a
multifactorial disease, and dietary lipids play an important role in biochemical and
physiological processes of vascular tissues and heart function. Thiery and Seidel [1] reported
that fish oil (FO) enhanced atherosclerosis in cholesterol (CHO)-fed rabbits, and Verschuren
et al [2] observed pathological lesions in the liver of fish-oil-fed rabbits. Dietary lipids are
known to induce extensive modification of fatty acid composition in cell membranes to
influence cellular functions [3].
Stanprans et al [4] postulated that dietary oxidized lipid (heated corn oil [HCO]) could be
atherogenic. Oxidized lipids are in many food products and intestinally derived lipoproteins
and endogenous lipoprotein particles such as very low-density lipoprotein and low-density
lipoprotein (LDL) could deliver these damaged lipids to tissues. Moreover, thermally
oxidized fat is generally considered to contain potentially toxic lipid peroxidation products
that would induce oxidative stress in animals [5].
Moghadasian and Frohlich [6] suggested that phytosterols in plant oils could inhibit
intestinal CHO absorption, thereby lowering plasma total and LDL CHO (LDL-C) levels.
However, this proposed action has not been thoroughly investigated. The effect of dietary
fatty acids on serum CHO levels and the development of atherosclerosis in animals have been
studied extensively, but little attention has been paid to the effect of oxidation status of dietary
oils on the development of atherosclerosis and lipid metabolism. The objective of the present
study was to determine the effects of oxidation status of dietary fat on atherosclerosis, blood
lipids, lipoprotein levels, and erythrocyte membrane fatty acid profiles in the rabbit.
2. Methods and materials
2.1. Animal diets and experimental protocol
Forty young male New Zealand White rabbits (average weight, 3 kg) were divided into
5 groups and individually housed in stainless steel cages. Each group was assigned to
treatments to equalize body weight by a restricted randomization technique during the 12-week
feeding experiment. After 1 week of acclimation, each group of rabbits was fed a commercial
rabbit chow with one of the following treatment additions (g/kg diet): 1.5 g CHO, 20 g corn oil
(CO) + 1.5 g CHO, 20 g FO (menhaden oil) + 1.5 g CHO, 20 g oxidized oil (OO) + 1.5 g CHO,
or 20 g HCO + 1.5 g CHO. Both CHO and oil were dissolved in 99.9% chloroform to make each
treatment and sprayed onto a basal rabbit chow as a fine mist. The amount of CHO and oil in
chloroform was adjusted to provide the desired concentration of CHO in each test diet. The
distribution of CHO was confirmed by CHO and oil analyses of the diets. Chloroform was
evaporated by exposing the diets in thin layer at 228C overnight in well-ventilated fume hood.
Butylathydroxytoluene (BHT) (0.02% of diet) was added to minimize oxidation of lipid and
CHO during chloroform evaporation and subsequent storage of the diet. The nutrient content of
the basal diet and the fatty acid composition and peroxide value (PV) of oils used in this study
are shown in Tables 1 and 2. Daily portions of diets were individually vacuum-packaged and
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
927
Table 1
Nutrient content of basal diet rabbit chow
Nutrient
Amount (%)
Crude protein (minimum)
Crude fat (minimum)
Crude fiber (minimum)
Calcium (minimum)
Phosphorous (minimum-maximum)
Salt (NaCl) (minimum-maximum)
Vitamin A (minimum)
16.0
1.5
17.0
20.0
0.6-1.1
0.5-1.0
4400 IU/kg
Ingredients: processed grain by-products, forage products, roughage products, plant protein products, grain
products, molasses products, calcium carbonate, salt, ferrous oxide, DL-methionine, choline chloride, vitamin E
supplement, calcium pantothenate, vitamin B12 supplement, niacin supplement, vitamin A supplement, manganese
sulfate, vitamin D3 supplement, ferrous sulfate, cobalt carbonate, calcium iodate, copper sulfate, zinc sulfate,
magnesium oxide, and sodium selenite.
stored in a freezer ( 208C) to prevent oxidative changes. After a week of adaptation, rabbits
were fed the experimental diets (170 g/d per rabbit) for 12 weeks. Blood samples were taken
from the ear vein every 3 weeks. Four rabbits per treatment were euthanized by a pentobarbital
overdose (200 mg/kg body weight) at days 63 and 84 of the feeding study. After blood
sampling, the thorax was opened and aorta samples were collected. The feeding, sample
collection, and euthanasia protocols were approved by the Animal Care Committee of Iowa
State University and complied with the Care and the Use of Laboratory Animals.
2.2. Preparation of oxidized and HCOs
Oxidized oil was prepared by washing a vegetable oil mix (CO and soybean oil purchased
from a local source) with ethanol (1:1, vol/vol) 10 times to remove all the tocopherols and
phytosterols in the oil. The oil was maintained at room temperature for 2 years before use.
Heated corn oil was prepared as follows: CO was poured into a glass beaker and heated for
48 hours on a hotplate set at constant temperature of 1508C with stirring. The extent of
peroxidation in oxidized and heated oils was determined by PV [7].
2.3. Histopathology
Aorta sections were evaluated by light microscopy to assess pathology. Aortas were fixed
in 10% buffered formalin for 24 hours, tissues were trimmed, and 4 cross sections of aorta
were placed on 1 block. Tissues were washed for 4 hours in tap water, dehydrated in an
automated processor (Pathcentre Processor, ThermoShandon, Pittsburgh, Pa) and embedded
in paraffin. Sections were cut at 5 lm and stained with hematoxylin and eosin to determine
the development of atherosclerosis in rabbits. Histologically, aortic lesions are composed of
very large, pale, vacuolar, lipid-filled macrophages. The lipid-filled macrophages of the
plaque are strongly positive for oil-red-O but does not stain with blue at acid pH or with the
periodic acid–Schiff procedure for glycoproteins/glycolipids. The severity of a lesion was
based on the histopathologic features of samples using a scoring system. The atherosclerotic
lesions was as follows: 0, no abnormality detected; 1+, focal aggregation of 4 to 8 foam cells
in the tunica intima; 2+, multifocal aggregates of foam cells and lipid; 3+, focally extensive
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S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
Table 2
Fatty acid composition and PVs of oils fed to rabbits
Component
CO
FO
OO
HCO
composition (weight %)
Fatty acid
Myristic acid
Palmitic acid
Palmitoleic acid
Oleic acid
Elaidic acid
Linoleic acid
Linolenic acid
Stearic acid
Eicosatetrenoic acid
Eicosapentanoic acid
Docosahexanoic acid
Other fatty acids
–
13.88 F
–
28.39 F
–
54.93 F
0.36 F
2.34 F
–
–
–
–
Peroxide value
30.28 F 1.12
0.02
0.22
0.23
0.05
0.08
7.56
20.19
10.11
10.74
0.68
1.70
3.31
3.45
0.65
12.23
11.72
25.90
F
F
F
F
F
F
F
F
F
F
F
F
0.16
0.32
0.24
0.25
0.06
0.06
0.09
0.07
0.03
0.19
0.20
0.39
–
10.63 F
–
37.15 F
–
50.15 F
–
2.06 F
–
–
–
–
0.25
0.56
0.94
0.13
mEq peroxide per kg of oil
31.57 F 0.66
144.87 F 8.15
–
13.82 F 0.15
–
33.55 F 0.15
1.11 F 0.07
49.17 F 0.15
–
2.34 F 0.08
–
–
–
–
28.43 F 0.59
Values are means F SD (n = 4).
thick layers of lipid and foam cells in the tunica intima extending part way around blood
vessels; and 4+, diffuse thick layer of lipids and foam cells infiltrating the tunica intima and
extending around the circumference of the blood vessel and bulging into the lumen. The total
area involved in subendothelial lesions was quantified by image analysis using microscopic
analysis and video capture to produce digitized images that were analyzed by PILab software.
The mean intimae thickness was calculated from measurements of the distance from the
luminal surface to the internal elastic lamina.
2.4. Analyses of CHO and triacylglycerol in plasma
Plasma CHO (kit no. 352-20 by Sigma Chemical Co, St Louis, MO) and triacylglycerols
(TGs; kit No. 339-20, Sigma Chemical Co) was determined using enzymatic assay kits as
specified by the manufacturers.
2.5. Analysis of fatty acids in erythrocytes
After decanting plasma, packed erythrocytes were homogenized with 10 volumes of
deionized distilled water and then centrifuged at 2000g for 15 minutes. The precipitant was
washed and centrifuged repeatedly until colorless ghost erythrocytes were obtained. Lipids
were extracted from the ghost red cells [8] and then dried under nitrogen gas. Hexane 1 mL
and 1 mL of methylating reagent were added to the 100 lL of lipid extract from red blood cell
and incubated in a 908C water bath for 1 hour. After cooling to room temperature, methylated
fatty acids were extracted with 2 mL hexane and 5 mL water and analyzed using a gas
chromatograph (HP 6890, Hewlett Packard Co, Wilmington, Del). The gas chromatograph
operating conditions were 1808C for 2.5 minutes, temperature programed to 2308C at 2.58C
per minute and held at 2308C for 7.5 minutes. The injector and detector were operated at
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
929
Table 3
Atherosclerotic lesions in aorta of rabbits fed diets containing CHO and different oils for 9 and 12 weeks
Dietary treatment
9 wk
NO
CO
FO
OO
HCO
2.25
1.00
2.25
1.75
1.00
12 wk
Score of lesions
F
F
F
F
F
0.50
0.82
1.15
0.82
0.50
3.75
1.50
2.75
3.50
1.50
F
F
F
F
F
0.50
0.82
0.82
0.58
0.50
Score of lesions (mean F SD, n = 4): 0, no abnormality detected; 1, focal aggregation of 4 to 8 foam cells; 2,
multifocal aggregates of foam cells and lipid; 3, focally extensive thick layers of lipid and foam cells in the tunica
intima extending part way around blood vessels; 4, diffuse thick layer of lipids and foam cells infiltrating the tunica
intima and extending around the circumference of the blood vessel and bulging into the lumen. NO, 0% oil; CO,
2% fresh corn oil; FO, 2% fresh fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg
diet) was added to all the experimental diets.
2808C. Helium was the carrier gas at linear flow of 1.1 mL/min. The flame ionization detector
was operated with air, H2, and make-up gas (helium) of 350, 35, and 43 mL/min, respectively.
Fatty acids were identified by the comparison of retention times to known standards, and
relative quantities were expressed as weight percentage of total fatty acids.
2.6. Statistical analysis
Data were analyzed using SAS software (SAS Institute Inc, Cary, NC) [9] by the
generalized linear model procedure. The Student-Newman-Keuls multiple range test was
used to compare differences among means. Mean values and SDs of the mean are reported.
Significance was defined at P b .05.
3. Results and discussion
The histopathologic data (qualitative) indicated that the rabbits receiving 0% oil (NO
group) and 2% FO resulted in the most severe atherosclerotic lesions, followed by the 2%
OO group; however, rabbits fed the 2% CO and 2% HCO had the least lesions in aorta after
9 weeks of feeding (Table 3). After 12 weeks, those in the NO and OO groups had the highest
lesions, the FO group was intermediate, and the CO and HCO groups had the least lesions.
The rabbits from CO and HCO groups developed mild focal aggregations (1+ severity), and
some increase in atherosclerotic lesions were found between rabbits necroscopied at 9 and
12 weeks (Table 3). The aorta of rabbits receiving NO, FO, and OO developed multifocal
aggregates of foam cells and lipids after 9 weeks, and the severity of lesions progressed
rapidly over the next 3 weeks of the study. The progression of atherosclerotic lesions in aorta
was fastest in OO group, followed by NO group and the FO group. The severity of lesions in
the NO and OO groups after 12 weeks were very high (N3.5+), and NO and OO group
developed thick layers of lipids and foam cells infiltrating the tunica intima extending part
way around the circumference of the blood vessels and bulging into the lumen. Lesions in the
aorta of rabbits from FO group developed focal thick layers of lipid and foam cells in the
tunica intima but were confined mainly to the tunica intima.
930
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
Table 4
Effect of various dietary oils on CHO content in plasma of rabbits
Dietary
treatment
NO
CO
FO
OO
HCO
Feeding period (wk)
0
69.6 F 6.5c
69.6 F 6.5d
69.6 F 6.5d
69.6 F 6.5d
69.6 F 6.5d
3
407.7
333.8
341.9
396.2
281.4
6
F
F
F
F
F
19.9b,w
16.6b,x
14.8c,x
22.8c,w
37.3a,y
447.1
379.0
429.1
444.9
246.0
9
(lg/dL)
F 21.8a,w
F 29.6a,x
F 25.5b,w
F 24.3b,w
F 34.35b,y
453.6
321.0
459.9
474.4
192.7
12
F
F
F
F
F
32.0a,w
15.6b,x
16.0a,w
20.0a,w
19.4c,y
430.6
281.8
449.8
435.8
184.4
F
F
F
F
F
29.8a,b,w
31.1c,x
27.8a,b,w
42.4b,w
27.5c,y
a, b, c, d and e
Values (means F SD, n = 4) within a row having different superscript letters are significant based on
feeding period ( P b .05). v, w, x, y, and z Values (means F SD, n = 4) within a column having different superscript
letters are significant based on dietary treatment ( P b .05). NO, 0% oil; CO, 2% fresh corn oil; FO, 2% fresh
fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg diet) was added to all the
experimental diets.
These results indicate that the dietary oils, which differ significantly in their fatty acid
compositions, degree of oxidation, and polymerization, could have different effect on the
development of atherosclerotic lesions in rabbits. The rapid progression of atherosclerotic
lesions in rabbits receiving OO, which had a high PV value, indicates that prolonged
exposure to oxidized oil is harmful. This is due to the oxidation of fatty acids and perhaps to
the removal of phytosterols. It is expected that CHO played an important role in the
development of atherosclerosis. The low degree of lesions in aorta from CO and HCO groups
suggests that polymerization of oil by heat treatment had little effect on the development of
atherosclerotic lesions in rabbits. Heating of CO did not increase PV but increased the
viscosity of the oil due to polymerization of oil (data not shown).
Dietary FO is reported to have a beneficial effect on the reduction of atherosclerotic lesions
and tissue CHO levels in the aorta and pulmonary artery [10]. Although the FO used in this
study had a similar PV value to CO and HCO, rabbits fed the FO diet developed more severe
atherosclerotic lesions than those fed CO and HCO after 9 and 12 weeks of feeding. Aguilera
et al [11] observed that the progression of atherosclerotic lesions was significantly influenced
by the source of dietary lipid: dietary olive oil led to lower lesions than FO, which produced
lower lesions than sunflower oil. Ritskes-Hoitinga et al [12] reported that the degrees of aortic
atherosclerosis in rabbits increased as the level of dietary FO increased. They also found that
long-term consumption of high levels of FO (10% and 20% energy) led to more severe aortic
atherosclerosis and did not demonstrate a beneficial effect on aortic atherosclerosis in rabbits.
Thiery and Seidel [1] found that feeding FO, which contains large amounts of omega-3 fatty
acids, to rabbits enhanced CHO-induced atherosclerosis and elevated serum peroxides.
Plasma total CHO levels increased markedly after 3 weeks of feeding the diets and reached
maxima after 6 or 9 weeks except for the HCO group, which reached its maximum after
3 weeks (Table 4). Kanakaraj and Singh [13] reported that feeding CHO to rabbits increased
CHO content in plasma and erythrocytes and caused an increased ratio of CHO/phospholipid.
The rabbits receiving NO, FO, and OO diets had the highest; CO diet, intermediate; and
HCO, the lowest plasma CHO levels among the treatments after 6 weeks of feeding (Table 4),
indicating that the development of atherosclerotic lesions is closely related to the plasma
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
931
Table 5
Effect of various dietary oils on triacylglycerols in plasma of rabbits
Dietary
treatment
NO
CO
FO
OO
HCO
Feeding period (wk)
0
21.3 F 1.5c
21.3 F 1.5d
21.3 F 1.5e
21.3 F 1.5e
21.3 F 1.5e
3
6
9
22.5 F 2.4c,y
22.9 F 2.7d,y
43.9 F 2.6d,w
38.1 F 2.1d,x
25.4 F 1.7d,y
(mg/dL)
34.8 F 1.5b,z
57.5 F 4.6c,w
47.5 F 2.5c,x
43.1 F 4.3c,y
35.8 F 3.0c,z
64.0
62.6
88.0
65.2
57.9
12
F
F
F
F
F
4.3a,x
4.0b,x
3.6b,w
3.86b,x
2.5b,x
67.7
78.7
98.3
94.9
64.7
F
F
F
F
F
2.4a,y
2.2a,x
2.5a,w
5.51a,w
3.0a,y
a, b, c, d and e
Values (means F SD, n = 4) within a row having different superscript letters are significant based on
feeding period ( P b .05). v, w, x, y, and z Values (means F SD, n = 4) within a column having different superscript
letters are significant based on dietary treatment ( P b .05). NO, 0% oil; CO, 2% fresh corn oil; FO, 2% fresh
fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg diet) was added to all the
experimental diets.
CHO level. Higher plasma CHO levels in rabbits fed the NO diet compared with the CO diet
indicates that dietary oil inhibits, whereas the degree of oxidation in oil increases, the
absorption of CHO. Kritchevsky et al [14] reported that dietary CO lowered the concentration
of CHO in rat serum, which is consistent with our results. The lowest plasma CHO observed
with the HCO diet in this study suggested that polymerization of CO by heating (HCO)
inhibited the absorption of dietary CHO, which, in turn, lowered the atherosclerotic lesions in
rabbits. Our results agree with those of Eder and Stangl [15] who demonstrated that feeding
thermoxidized oil lowered the concentrations of CHO in plasma.
Heinemann et al [16] reported that plant sterols decrease CHO absorption. Generally, an
elevated plasma CHO level is a major risk factor for cardiovascular disease [17]. In the
present study, the changes of plasma CHO levels in rabbits fed different dietary oils showed
similar trends in atherosclerotic lesions. Thus, it is probable that high plasma CHO is the
major factor involved in the development of atherogenic lesions in rabbits.
The TG content in plasma increased gradually in all rabbits as the feeding time increased
(Table 5). Rabbits from NO and HCO groups had the lowest plasma TG levels throughout the
feeding periods. The plasma TG levels of rabbits from the FO and OO groups doubled after
3 weeks, but rabbits from other groups showed slower changes in TG levels. The changes in
TG content among dietary CHO groups showed similar trends as in plasma CHO. Aguilera
et al [11] found that pigs receiving FO had a significantly lower serum TG concentration than
those receiving milk fat and coconut oil. Some reports in guinea pigs fed CHO in chow diets
containing CO or coconut oil [18] and in rabbits receiving coconut oil– or olive oil–based
diets [19] also had similar results. Paik and Blair [20] suggested that TG-rich lipoproteins are
not considered to be atherogenic, but they are related to the metabolism of high-density
lipoprotein (HDL) CHO (HDL-C) and indirectly to coronary heart disease.
The levels of LDL-C markedly increased after 3 weeks in all dietary groups (Table 6).
After 12 weeks, the plasma LDL-C level of rabbits from NO, FO, and OO groups were
significantly ( P b .05) higher than that of CO and HCO. The lowest level was in the HCO
group. The LDL-C showed similar trends as in plasma CHO levels and the degree of
atherosclerotic lesions in aorta. Aguilera et al [11] reported that a high CHO (1.5%) and lard
932
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
Table 6
Effect of various dietary oils on plasma LDL-C in rabbits
Dietary
treatment
NO
CO
FO
OO
HCO
Feeding period (wk)
0
3
52.7
52.7
52.7
52.7
52.7
F
F
F
F
F
6.4c
6.4d
6.4d
6.4d
6.4d
6
387.3
317.3
317.4
376.5
260.7
F
F
F
F
F
19.7b,w
15.5b,x
16.6c,x
22.8c,w
37.8a,y
9
426.1
361.6
401.3
425.6
225.5
lg/dL
F 22.3a,w
F 29.9a,x
F 25.5b,w
F 25.1b,w
F 33.5b,y
12
429.5
302.6
429.4
454.1
165.9
F
F
F
F
F
33.2a,w
15.4b,x
18.0a,w
19.8a,v,w
20.1c,y
401.4
261.9
419.3
414.2
157.6
F
F
F
F
F
31.0a,b,w
31.9c,x
26.8a,b,w
41.4b,w
27.7c,y
a, b, c, d and e
Values (means F SD, n = 4) within a row having different superscript letters are significant based on
feeding period ( P b .05). v, w, x, y, and z Values (means F SD, n = 4) within a column having different superscript
letters are significant based on dietary treatment ( P b .05). NO, 0% oil; CO, 2% fresh corn oil; FO, 2% fresh
fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg diet) was added to all the
experimental diets.
(3.5%) diet for 50 days increased plasma total and LDL-C levels and increased LDL
susceptibility to oxidation in pigs. Oxidized lipoproteins play an important role in the
development of atherosclerosis, and thus, the susceptibility of LDL to peroxidation is of great
importance to heart disease [21]. In the present study, we also found that the dietary oils
influenced the LDL-C level, and elevated LDL-C was associated with greater atherogenic
lesions in rabbits.
The plasma HDL-C level in all rabbits gradually increased ( P b .05) after the duration of
the study (Table 7). After 12 weeks of feeding, the level of plasma HDL-C in NO and FO was
significantly higher ( P b .05) than that of other treatments. Low-density lipoprotein is
considered as an atherogenic lipoprotein, whereas HDL antagonizes atherogenic potential.
Paik and Blair [20] reported that HDL is needed to protect against atherosclerosis only when
LDL is atherogenic. They also suggested that the HDL changes were inconsistent and varied
from subject to subject. Thornburg et al [22] reported that the quantity of CHO within HDL is
Table 7
Effect of various dietary oils on plasma HDL-C in rabbits
Dietary
treatment
0
NO
CO
FO
OO
HCO
16.2
16.2
16.2
16.2
16.2
a, b, c, d and e
Feeding periods (weeks)
3
F
F
F
F
F
1.3d
1.3c
1.3d
1.3c
1.3c
20.4
16.5
24.3
19.7
20.7
6
F
F
F
F
F
1.2c,w
1.3c,x
1.9c,v
1.4b,w
1.8b,w
20.9
17.4
27.8
19.4
20.9
9
lg/dL
F 1.1c,x
F 1.2b,c,y
F 1.7b,v
F 1.4b,x
F 1.4b,x
24.1
18.4
30.0
20.4
26.7
12
F
F
F
F
F
1.8b,x
1.3b,z
2.4a,v
1.2a,b,y
1.8a,w
29.2
20.0
30.5
21.6
26.8
F
F
F
F
F
2.0a,v
1.6a,w
2.4a,v
2.1a,w
3.1a,w
Values (means F SD, n = 4) within a row having different superscript letters are significant based on
feeding period ( P b .05). v, w, x, y, and z Values (means F SD, n = 4) within a column having different superscript
letters are significant based on dietary treatment ( P b .05). NO, 0% oil; CO, 2% fresh corn oil; FO, 2% fresh
fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg diet) was added to all the
experimental diets.
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
933
Table 8
Fatty acid composition of RBC membranes in rabbits
Fatty acid
NO
CO
Myristic acid
Palmitoleic acid
Palmitic acid
Margaric acid
Linoleic acid
Oleic acid
Linolenic acid
Stearic acid
Arachidonic acid
Eicosapentaenoic acid
Docosahexaenoic acid
Unidentified
SFA/USFA
0.48b
0.97b
25.66b,c
0.82b
29.89a
17.95a,b
1.81a
15.65c,d
5.45a
0b
0b
1.32c
41.8/56.9
0c
0.68c
25.37b,c
0.63c
32.71a
15.70b,c
1.50b
17.99a,b
4.28b
0b
0b
1.19c
43.4/55.5
FO
(weight %)
0.68a
1.84a
29.17a
1.27a
20.01b
14.45c
1.87a
18.99a,b
4.75b
3.11a
2.05a
1.86a
48.8/49.4
OO
HCO
0.45b
1.02b
24.24c
0.25d
31.45a
20.92a
1.42b
15.03d
3.98b
0b
0b
1.27c
39.7/59.0
0.47b
0.59c
27.41b
0.32d
32.38a
14.45c
1.45b
17.11b,c
4.48b
0b
0b
1.36c
45.0/53.6
a, b, c, d and e
Values (means F SD, n = 4) within a row having different superscript letters are significant based on
feeding period ( P b .05). v, w, x, y, and z Values (means F SD, n = 4) within a column having different superscript
letters are significant based on dietary treatment ( P b .05). NO, 0% oil; CO, 2% fresh corn oil; FO, 2% fresh
fish oil; OO, 2% oxidized oil; HCO, 2% heated corn oil. Cholesterol (1.5 g/kg diet) was added to all the
experimental diets.
SFA= saturated fatty acid; USFA= unsaturated fatty acid.
dependent upon the activity of lecithin, CHO acyl transferase, which, in turn, is dependent
upon the composition of phosphatidylcholine within HDL. Aguilera et al [11] found that
changes in the amount of total CHO in pigs are more likely to reflect the changes in serum
HDL than LDL concentrations. Moreover, Paik and Blair [20] reported that high consumption
of CHO tended to increase the levels of HDL as well as LDL.
Dietary oils significantly influenced by the fatty acid composition of erythrocyte (RBC)
membranes as would be expected (Table 8). Dietary NO and OO treatments increased the
levels of unsaturated fatty acids and decreased saturated fatty acids. Fish oil changed the fatty
acid composition of RBC membrane the most among the dietary oil treatments. Amounts of
palmitoleic, palmitic, margaric, stearic, eicosapentaenoic, and docosahexaenoic acids of RBC
membranes of rabbits fed FO were the highest, and linoleic and oleic acids were the lowest in
this group, compared with the other oil treatments. The fatty acid composition of serum lipids
reflected the compositions of dietary lipids and oils well [23]. Porsgaard and Carl-Erik [24]
reported that the fatty acid composition and structure of dietary fat influenced the digestion
and absorption of fat. Jorgensen et al [25] reported that dietary fats from animal sources had a
lower digestibility and energy value than those from vegetable sources due to higher content
of saturated fatty acids (16:0 and 18:0).
In conclusion, plasma total CHO level was the most critical factor involved in the
development of atherogenic lesions in the rabbit. Dietary CHO and oxidation status of dietary
lipids had a significant impact on lipid metabolism and the development of atherosclerotic
lesions in rabbits. Dietary oxidized oils accelerate the progression of atherosclerotic lesions,
but polymerization of oils by heating lowered plasma CHO level and the development of
atherogenic lesions in rabbits. Heated oils may inhibit the absorption of CHO.
934
S.J. Hur et al. / Nutrition Research 25 (2005) 925 – 935
Acknowledgment
This research was supported by the Iowa Egg Council.
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