Biochimica et Biophysica Acta 1761 (2006) 345 – 349
http://www.elsevier.com/locate/bba
Structured triglycerides containing caprylic (8:0) and oleic (18:1)
fatty acids reduce blood cholesterol concentrations and aortic
cholesterol accumulation in hamsters
Thomas A. Wilson a , David Kritchevsky b , Timothy Kotyla a , Robert J. Nicolosi a,⁎
a
Department of Clinical Laboratory and Nutritional Sciences, Center for Health and Disease Research, University of Massachusetts Lowell,
3 Solomont Way, Suite 4, Lowell, MA 01854, USA
b
Wistar Institute, Philadelphia, PA 19104, USA
Received 26 August 2005; received in revised form 2 February 2006; accepted 23 February 2006
Available online 20 March 2006
Abstract
The effects of structured triglycerides containing one long chain fatty acid (oleic acid, C18:1) and one short chain saturated fatty acid (caprylic
acid, 8:0) on lipidemia, liver and aortic cholesterol, and fecal neutral sterol excretion were investigated in male Golden Syrian hamsters fed a
hypercholesterolemic regimen consisting of 89.9% commercial ration to which was added 10% coconut oil and 0.1% cholesterol (w/w). After 2
weeks on the HCD diet, the hamsters were bled, following an overnight fast (16 h) and placed into one of three dietary treatments of eight animals
each based on similar plasma cholesterol levels. The hamsters either continued on the HCD diet or were placed on diets in which the coconut oil was
replaced by one of two structured triglycerides, namely, 1(3),2-dicaproyl-3(1)-oleoylglycerol (OCC) or 1,3-dicaproyl-2-oleoylglycerol (COC) at
10% by weight. Plasma total cholesterol (TC) in hamsters fed the OCC and COC compared to the HCD were reduced 40% and 49%, respectively
(P < 0.05). Similarly, hamsters fed the OCC and COC diets reduced their plasma nonHDL cholesterol levels by 47% and 57%, respectively
(P < 0.05), compared to hamsters fed the HCD after 2 weeks of dietary treatment. Although hamsters fed the OCC (−26%) and COC (−32%) had
significantly lower plasma HDL levels compared to HCD, (P < 0.05), the plasma nonHDL/HDL cholesterol ratio was significantly lower (P < 0.05)
compared to the HCD for the OCC-fed (−27%) and the COC-fed (−38%) hamsters, respectively. Compared to the HCD group, aortic esterified
cholesterol was 20% and 53% lower for the OCC and COC groups, respectively, with the latter reaching statistical significance, P < 0.05. In
conclusion, the hamsters fed the structured triglyceride oils had lower blood cholesterol levels and lower aortic accumulation of cholesterol
compared to the control fed hamsters.
© 2006 Elsevier Inc. All rights reserved.
Keywords: Structured triglycerides; Oleic acid; Plasma cholesterol; Aortic cholesterol; Hamsters
1. Introduction
There is evidence that the specific structure of triglycerides
may influence their effects of experimental atherosclerosis. It
has been shown that the randomization of fats can decrease [1]
or increase [2] the amount of palmitic acid at the SN2 position,
which can decrease [1], increase [2] or have no effect (Nicolosi et
al., unpublished results cited in [3]) on their atherogenicity. In
the review by Hunter [3], both experimental studies in animals
and human clinical trials, indicate that interesterified fats
⁎ Corresponding author. Tel.: +1 978 934 4501; fax: +1 978 934 3025.
E-mail address: [email protected] (R.J. Nicolosi).
1388-1981/$ - see front matter © 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.bbalip.2006.02.019
involving palmitic acid (C16:0), stearic acid (C18:0) and oleic
acid (C18:1) have not shown any significant effects on blood
lipid parameters. For example, the animal studies by Kritchevsky et al. [1,2,4–6] in rabbits and one unpublished study by
Nicolosi et al. in hamsters cited by Hunter [3], showed no effects
of inter-esterified fats on plasma total and lipoprotein cholesterol. Similarly, studies by Zock et al. [7], Nestel et al. [8,9], and
Meijer and Weststrate [10] in humans demonstrated no
significant effects of inter-esterified fats on plasma total and
lipoprotein cholesterol levels.
While there have been studies demonstrating the hypocholesterolemic effect of medium chain triglycerides (MCT) which
contain mostly caprylic (C8:0) or capric (C10:0) fatty acids in
346
T.A. Wilson et al. / Biochimica et Biophysica Acta 1761 (2006) 345–349
rats [11], dogs [12], and humans [13] compared to triglycerides
containing longer chain saturated fatty acids and one study
showing that MCT are also significantly less atherogenic than
coconut oil for cholesterol-fed rabbits [14], the influence of
C8:0 fatty acids on the cholesterolemic properties of structured
triglycerides has not been investigated.
Therefore, the effects of structured triglycerides containing
one long chain fatty acid (oleic, C18:1)) and one short chain
saturated fatty acid (caprylic 8:0) on lipidemia, liver and aortic
cholesterol and fecal neutral sterol excretion was investigated in
hamsters.
2. Methods
2.1. Experimental design and diets
Twenty-four 10-week-old Golden Syrian hamsters were purchased from
Charles River Laboratories (Wilmington, MA) and placed on a commercial
ration (Purina, St. Louis MO) for 1 week. The hamsters were then placed on a
hypercholesterolemic regimen consisting of 89.9% commercial ration (Purina
Laboratory Rodent Diet 5001, Purinal, St. Louis, MO), 10% coconut oil and
0.1% cholesterol. The commercial ration contained 4.5% total fat by weight
including linoleic acid (1.16%), linolenic acid (0.07%), eicosapentenoic and
docosahexenoic acids (0.26%), total saturated fatty acids (1.5%), and total
monounsaturated fatty acids (1.58%). The HCD used in this study has been
shown by us [15] and others [16] to be more hyperlipidemic than semi-purified
diets for hamsters. After 2 weeks on the HCD diet, the animals were bled,
following an overnight fast (16 h) and divided into three groups of eight animals
each based on similar plasma cholesterol levels. The hamsters either continued
on the HCD or placed on diets in which the coconut oil had been replaced by one
of two structured triglycerides, namely, 1(3),2-dicaproyl-3(1)-oleoylglycerol
(OCC) or 1,3-dicaproyl-2-oleoylglycerol (COC) at 10% by weight. The test
triglycerides were prepared by The Nisshin Oil Mills, Kanagawa, Japan using a
proprietary enzymatic method for inter-esterifying tricaprylin with oleic and to
give OCC or triolein with caprylic acid to give COC. The molecular profiles of
the two test fats are detailed in Table 1. Food disappearance and body weights
were measured on daily basis throughout the study. The animals were
maintained in accordance with the guidelines of the Committee on Animal
Care of the University of Massachusetts Lowell Research Foundation, and the
guidelines prepared by the Committee on Care in Use of Laboratory Animals of
the Institute of Laboratory Resources, National Research Council (DHEW
publication no. 85-23, revised 1985) following approval by the Institutional
Animal Care and Use Committee for approval.
2.2. Plasma lipoprotein cholesterol and triglyceride measurements
Blood samples taken from fasted (16 h) hamsters at weeks 0, 1, and 2 under
CO2:O2 (50/50) gas (Northeast Airgas, Salem, NH) anesthesia, were collected
Table 1
Molecular species (%) in test oils (OCC) and (COC)
2.3. Collection of aortas and aortic cholesterol measurement
At the end of the 2 weeks, hamsters were anesthetized with an IP injection of
sodium pentobarbital (62.5 mg/mL at a dosage of 0.2–0.25 mL/200 gram body
weight) (Henry Schein, Port Washington, NY) and aortic tissue was obtained for
cholesterol analysis as previously stated [20]. The heart and thoracic aorta were
removed and stored in vials containing PBS at 4 °C for subsequent analysis. To
measure the extent of the aortic cholesterol accumulation in the aortic arch, a
piece of thoracic aortic tissue extending from as close to the heart as possible to
the branch of the left subclavian artery was used. Aortic total and free cholesterol
concentrations were determined enzymatically utilizing Wako Chemistry kits
(Wako Chemicals, Richmond, VA). Aortic cholesteryl ester concentration was
determined as the difference between the total and the free cholesterol
concentrations. This assay has been used successfully for analysis of hamster
tissue lipids [21].
2.4. Hepatic cholesterol measurement
Hepatic cholesterol concentrations were measured using previously
described methods [22,23]. After the whole liver was removed, a small portion
(100 mg) of the lower right lobe was used for all analyses of cholesterol
composition in each hamster.
2.5. Fecal neutral sterol measurement
Fecal samples were collected over the final 3 days of the exposure period,
freeze-dried (lyophilized), and ground prior to analysis. Concentrations of total
fecal cholesterol, and total and individual neutral sterols (coprostanol,
campesterol, β-sitosterol, β-sitostanol) were determined as described previously
[24] and based on the use of external standards available.
2.6. Statistical methods
Sigmastat software (Jandel Scientific, San Rafael, CA) was used for all
statistical evaluations [25]. A repeated measures one-way analysis of variance
(RM ANOVA) was used to analyze the data between groups. When statistical
significance was found by RM ANOVA, the Student–Newman–Keuls
separation of means was used to determine group differences. All values are
expressed as mean ± S.E.M. and statistical significance was set at P < 0.05.
3. Results
Molecular Species
OCC
COC
CCC
COC
OCC
COO
CLC
LCC
LLC
Others
4.6
–
84.7
4.7
–
–
–
6.0
2.4
38.4
31.4
10.7
2.9
2.4
0.9
10.9
C = Caprylic acid.
O = Oleic acid.
L = Linoleic acid.
into heparinized tubes via the retro-orbital sinus. Plasma was obtained after
centrifugation at 1500×g at room temperature for 10 min and total cholesterol
[17] and triglyceride [18] concentrations were determined enzymatically.
Plasma nonHDL-cholesterol, a combination of VLDL, intermediate and LDLC, was precipitated using a phosphotungstate reagent [19] and the high-density
lipoprotein cholesterol (HDL-C) was measured in the supernatant. Plasma
nonHDL-C was calculated as the difference between TC (total cholesterol) and
HDL-C. The accuracy of the procedures used for the measurement of plasma
total cholesterol, HDL-C, and triglycerides are maintained by participation in the
Lipid Standardization Program of the Center for Disease Control and the
National Heart, Blood, and Lung Institute.
The hamsters adapted well to all diets and all hamsters
survived the dietary treatments. Table 2 shows that there were
no differences among the groups in final body weight, liver
weight or liver index (liver wt/body wt).
No differences were observed between week 1 and week 2
for blood lipid and lipoprotein cholesterol levels, thus, they
were averaged together and the mean lipid findings are detailed
in Table 3. Plasma total cholesterol (TC) in hamsters fed the
OCC and COC compared to the HCD were reduced 40% and
49%, respectively (P < 0.05). Similarly, hamsters fed the OCC
T.A. Wilson et al. / Biochimica et Biophysica Acta 1761 (2006) 345–349
Table 2
Final body weight and liver weight of hamsters after 2 weeks of consuming the
HCD a
Final body weight (g)
Liver weight (g)
Liver index (%)
Control
OCC
COC
113.7 ± 1.1
5.38 ± 0.08
4.74 ± 0.11
115.3 ± 1.9
5.45 ± 0.14
4.72 ± 0.08
119.7 ± 2.8
5.78 ± 0.24
4.83 ± 0.11
Liver index = liver weight as % of body weight.
a
Values are mean ± S.E.M.; n = 8.
Table 3
Plasma lipid levels (mg/dL) of hamsters fed various fats for 2 weeks after
establishing hypercholesterlemia a,b
Total cholesterol
nonHDL-C
HDL-C
Triglycerides
a
Control
OCC
COC
443.2 ± 47.7 a
305.7 ± 20.6 a
138.0 ± 30.5 a
291.4 ± 46.3
264.8 ± 13.4 b
163.8 ± 11.9 b
101.4 ± 5.6 b
285.4 ± 41.6
226.4 ± 8.2 b
130.2 ± 8.7 b
95.2 ± 4.6 b
193.7 ± 22.8
Values are mean ± S.E.M.; n = 8.
Values in a row not sharing a lowercase superscript across treatments are
significantly different at P < 0.05.
b
Table 4
Liver cholesterol levels (mg/g of tissue) of hamsters fed various fats for 2 weeks
after establishment of hypercholesterolemia a
Total Cholesterol
Free Cholesterol
Esterified Cholesterol
% Esters
a
and COC diets reduced their plasma nonHDL cholesterol levels
by 47% and 57%, respectively (P < 0.05), compared to hamsters
fed the HCD after 2 weeks of dietary treatment. Although
hamsters fed the OCC (−26%) and COC (−32%) had
significantly lower plasma HDL levels compared to HCD,
(P < 0.05), the plasma nonHDL/HDL cholesterol ratio was
significantly lower (P < 0.05) compared to the HCD for the
OCC-fed (−27%) and the COC-fed (−38%) hamsters, respectively, (data not shown). No differences were observed between
the dietary treatments for plasma triglyceride concentrations.
Liver cholesterol values show that total liver cholesterol
was about 15% lower in the control group compared to the
test groups but not significantly (Table 4). The difference was
manifested primarily in the levels of esterified liver cholesterol. The percent liver cholesterol ester for the three
groups was 75.2 ± 0.10.
Table 5 shows that compared to the HCD-fed hamsters,
aortic total cholesterol was significantly reduced by 21% and
42%, (P < 0.05), respectively, for the OCC and COC-fed
animals. Also, compared to the OCC group, animals fed the
COC had 26% (P < 0.05) less aortic total cholesterol. Aortic free
cholesterol was 23% and 26% (P < 0.05) lower for the OCC and
COC groups, respectively, compared to the HCD group.
Compared to the HCD group, aortic esterified cholesterol was
20% and 53% lower for the OCC and COC groups, respectively
with the latter reaching statistical significance, (P < 0.05).
Compared to the OCC group, animals fed the COC diet had
41% (P < 0.05) less aortic esterified cholesterol. Animals fed the
COC diet had on average 81% (P < 0.05) greater free/esterified
cholesterol ratios compared to the HCD and COC diets. The %
aortic esterified cholesterol ranged from 50 to 60% across the
three diet treatments.
Table 6 presents the levels of neutral steroids excreted by
three test groups. Fat and cholesterol absorption were the same
in the three groups being 97.4 ± 0.21 and 72.2 ± 1.45%,
347
Control
OCC
COC
7.19 ± 0.71
1.73 ± 0.11
5.46 ± 0.66
75.7 ± 1.67
8.45 ± 1.24
1.81 ± 0.12
6.64 ± 1.12
76.6 ± 2.93
8.22 ± 1.20
1.94 ± 1.20
6.28 ± 1.06
73.4 ± 4.01
Values are mean ± S.E.M.; n = 8.
respectively. The major neutral sterols in all three groups
were campesterol and coprostanol.
4. Discussion
Medium chain triglycerides (MCT) were at one time
considered a possible substitute for dietary long chain
triglycerides but their use was eventually abandoned partially
because they elevated triglyceride levels. An excellent review of
the literature on MCT is available [26].
Interest then turned to the effects of mixed triglycerides
which might have the serum cholesterol effects of MCT but still
provide long chain polyunsaturated fatty acids. Jandacek et al.
[27] measured the rates of in vitro hydrolysis and absorption
from intestinal loops of CLC (2 linoleoyl-1, 3-dioctanoylglycerol) and OLO (2 linoleoyl-1, 3-diolegylglycerol). CLC was
hydrolyzed at a greater rate than MCT or OLO. Their study [27]
demonstrated the rapid hydrolysis and ease of absorption of
triglycerides carrying octanoic acids at the 1 and 3 positions and
linoleic acid at the second position.
Mu and Hoy [28,29] studied absorption of structured
triglycerides in rats: MCT are absorbed principally via the
portal vein and longer chain fatty acids via the lymphatic
system. Thus, they found lymphatic transport of 12:0/18:2/
12:0 > 10:0/18:2/10:0 > 8:0/18:2/8:0. They concluded that triglycerides containing medium chain fatty acids may be
hydrolyzed and the free medium chain fatty acids absorbed
via the portal blood but they are also absorbed by the same
pathway as long chain triglycerides involving hydrolysis to free
fatty acids, absorbed and eventually reacetylated into triacylglycerols. Tso et al. [30] compared absorption of 18:2/18:2/
18:2, 8:0/18:2/8:0 and 8:0/8:0/18:2 in rats Octanoate as free
fatty acid or 2-monoglyceride was absorbed rapidly and
transported via the portal vein. Skeda et al. [31] studied the
Table 5
Aortic cholesterol levels (μg/mg of tissue) of hamsters fed various fats for 2
weeks after establishment of hypercholesterolemia a, b
Total Cholesterol
Free Cholesterol
Esterified
Cholesterol
Free/Ester
% Esters
a
Control
OCC
COC
4.28 ± 0.40 a
1.72 ± 0.13 a
2.56 ± 0.32 a
3.34 ± 0.11 b
1.31 ± 0.11 b
2.03 ± 0.07 a
2.47 ± 0.19c
1.27 ± 0.17 b
1.20 ± 0.20 b
0.73 ± 0.04 a
59.2 ± 2.37
0.69 ± 0.07 a
60.9 ± 2.32
1.29 ± 0.35 b
50.0 ± 4.82
Values are mean ± S.E.M.; n = 8.
Values in a row not sharing a lowercase superscript across treatments are
significantly different at P < 0.05.
b
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T.A. Wilson et al. / Biochimica et Biophysica Acta 1761 (2006) 345–349
Table 6
Fecal neutral sterol levels and lipid absorption of hamsters fed various fats for 2
weeks after establishment of hypercholesterolemia a
Control
OCC
COC
Feces (g/3 days)
Fat absorption (%)
Cholesterol absorption (%)
3.4 ± 0.2
97.6 ± 0.25
73.0 ± 2.72
3.5 ± 0.2
97.1 ± 0.27
73.6 ± 2.63
4.0 ± 0.1
97.4 ± 0.31
70.1 ± 0.68
Neutral sterols (mg/g)
Coprostanol
Coprostanone
Cholesterol
Stigmasterol
β-Sitosterol
β-Sitostanol
Total
1.50 ± 0.15
0.13 ± 0.01
0.64 ± 0.06
0.15 ± 0.01
0.64 ± 0.04
0.48 ± 0.03
5.17 ± 0.32
1.04 ± 0.07
0.12 ± 0.02
0.59 ± 0.07
0.13 ± 0.01
0.64 ± 0.07
0.49 ± 0.03
4.57 ± 0.28
1.24 ± 0.15
0.13 ± 0.01
0.52 ± 0.05
0.14 ± 0.01
0.65 ± 0.05
0.44 ± 0.44
4.80 ± 0.31
a
Values are mean ± S.E.M.; n = 6.
effects of a number of triglycerides (18:2/18:2/18:2; 8:0/8:0/8:0,
8:0/18:2/8:0, 18:2/8:0/18:2, 10:0/10:0/10:0, 10:0/18:2/10:0,
18:2/10:0/18:2) on cholesterol absorption in rats and found no
significant differences.
In the work reported here, OCC and COC led to reductions of
plasma total and nonHDL cholesterol levels in the hypercholesterolemic hamsters but triglyceride levels were elevated in
both control and test groups. In view of the insignificant effects
of structured triglycerides containing palmitic, stearic and oleic
acids on plasma total and lipoprotein cholesterol in experimental
animals such as rabbits [1,2,4–6] and the unpublished studies in
hamsters cited in [3], our findings that OCC and COC structured
triglycerides can significantly reduce blood cholesterol levels is
exciting and warrants further study. The feeding of glycerides of
different structure has, to date, concentrated on effects of lipid
transport. We now show that in addition to affecting serum
lipids, the different triglycerides can influence severity of
atherosclerosis. Liver cholesterol levels were not significantly
different among the three groups. Aortic total cholesterol levels
were reduced by 22 and 42% in the hamsters fed OCC and COC,
respectively. Thus, the specific structural differences of the test
triglycerides were manifested in levels of plasma and aortic lipid
but not in liver lipids. This is not unexpected, since the short
chain fatty acids are absorbed via the portal system. The results
do suggest, however, that extrahepatic metabolism may play a
role in atherogenesis.
The amount of esterified aortic cholesterol was the same in
the control group and in the hamsters fed 088 but it was
significantly reduced in hamsters fed COC (53% lower than
controls and 49% lower than hamsters fed OCC). The level of
aortic ester cholesterol is a good indicator of atherogenicity.
Smith [32] showed that the level of cholesteryl ester in human
aortas increased with increasing age and atherosclerotic
involvement. Newman and Zilversmit [33] demonstrated the
same phenomenon in rabbits.
Our observation of reduced aortic cholesteryl ester only in
hamsters fed COC shows a specific difference in atherogenicity between OCC and COC. This difference would not have
been adduced from the serum or liver lipid levels. Assuming
the usual pattern of triglyceride absorption, the difference in
aortic cholesteryl ester accumulation could be due to
differences in 2-octanoyl vs. 2-oleolyn monoglycerides
which would lead to triglycerides containing predominately
8:0 or 18:1 at the SN2 position. The effect of triglyceride
structure on aortic cholesterol metabolism irrespective of
effects on serum and liver paramedics is a new observation
and one worth pursuing. This is an area of special importance
since, with the universal attempts to reduce or eliminate
intake of trans fats, it offers another avenue of approach, in
which measurement of aortic atheroslcerosis is as important
as measuring plasma lipids.
Acknowledgements
This project was funded by Nisshin Oil Mills LTD (RJN) and
by a Research Career Award (HL 00734) to Dr. David
Kritchevsky from the National Institute of Health (USA). The
authors would like to thank Toshi Aoyama, of Nisshin Oils,
Benjamin Woolfrey, Catherine Jones, and Subbiah Yoganathan
for the technical support and Maureen Faul and Laura Saba for
their administrative support.
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