![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Instituto de la Grasa, Consejo Superior de Investigaciones Cientificas, 41012 Sevilla, Spain and * Hospitales Universitarios Virgen del Rocío, 41013 Sevilla, Spain
2To whom correspondence and reprint requests should be addressed. E-mail: valruiz{at}cica.es.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
KEY WORDS: • monounsaturated oils • triacylglycerol • postprandial • minor fatty acids • humans
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
,2)
, case-control studies (3
,4)
and
several clinical conditions (5)
have related atherogenesis
and the metabolism of triacylglycerol-rich lipoprotein particles
(TRL),3
including chylomicrons, VLDL and their remnants. However, available
data support the view that not all TRL have atherogenic potential. In
recent studies, the substitution of dietary saturated fatty acids (SFA)
with monounsaturated fatty acids (MUFA) derived from olive oil improved
postprandial lipid metabolism and thrombotic response in humans
(6
,7)
.
TRL remnants are formed in the circulation when apolipoprotein (apo)
B-48, containing chylomicron of intestinal origin, or apo B-100,
containing VLDL of hepatic origin, are converted by lipoprotein lipase
(LPL) into smaller and more dense particles, i.e., those depleted of
triacylglycerols (TAG). The clearance of lipoprotein particles in
plasma can be regulated by the activity of lipases, cell surface
proteoglycans (8
,9)
and by factors that are responsible
for TRL remnant uptake such as receptor-mediated processes
(10
,11)
. It has been suggested that the stereospecific
structure of TAG may modify the clearance of TRL remnants from plasma
(12)
.
MUFA-rich oil consumption has been one of the recommended strategies
for modulating the plasma lipid profile in humans (13)
.
Two sources of MUFA, virgin olive oil (VOO) and high oleic sunflower
oil (HOSO), have been suggested to reduce the risk for cardiovascular
heart diseases by having a similar effect in diminishing the
atherogenic index (total cholesterol/HDL cholesterol) and LDL:HDL
cholesterol ratio in plasma of normocholesterolemic and
hypercholesterolemic hypertensive patients (14
,15)
.
However, the two MUFA-enriched diets (VOO and HOSO) had selective
physiologic effects in humans (16
,17)
. These studies
highlight the fact that other factors such as TAG composition, minor
fatty acids and nonfatty acid constituents, rather than the content of
oleic acid, might be responsible for the benefits of VOO intake in
healthy subjects and patients with cardiovascular risk factors
(18)
.
The aim of this study was to evaluate the postprandial TAG response in TRL of Svedberg flotation rate (Sf) > 400 in normolipidemic subjects after the ingestion of two MUFA-rich oils (VOO and HOSO) with equal amounts of oleic acid but different compositions of minor fatty acids and TAG molecular species. As far as we know, this is the first study to show the analysis of TAG molecular species in humans during the postprandial period after the ingestion of different dietary oils.
|
SUBJECTS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Virgin olive oil (v. cornicabra) was kindly supplied by Aceites Toledo
SA, Los Yébenes, Toledo, Spain. High oleic sunflower oil was
obtained from a local grocery store. The oils had the same MUFA
concentration (g/100 g total fatty acids) but differed in
polyunsaturated fatty acid (PUFA) and SFA amounts (Table 1
).
|
Eight normolipidemic men were asked to participate in the study. They
did not suffer from any digestive or metabolic disease as verified by
medical history. Plasma chemistry and hematologic indices were within
the normal range for all of the men. Age, body mass index, and baseline
blood lipid and lipoprotein concentrations are listed in Table 2
. The subjects gave written, informed consent to a protocol approved by
the Institutional Committee on Investigation in Humans (Hospitales
Universitarios Virgen del Rocío, Sevilla).
|
The study was designed as a short-term double-blind study. On
separate occasions, the men ingested three meals with 2 wk between
meals. All subjects maintained their habitual free-living diet
during this period. In randomized order, the subjects were given the
following: 1) one slice of brown bread (28 g); 100 g of
plain pasta (cooked with 200 mL water); 130 g of tomato sauce and
one skimmed yogurt, providing 1936 kJ of energy (control meal);
2) the control meal plus 70 g of virgin olive oil (4523
kJ of energy); and 3) the control meal plus 70 g
of the high oleic sunflower (4523 kJ of energy). The oils were
supplied mixed with the tomato sauce and the subjects could not tell
which oil they were eating (19)
. The dose of oil
administered was similar to that used in previous human studies
(20
,21)
.
On the day of the postprandial study, the men were asked to consume a
low fat meal, to refrain from smoking and drinking alcohol during the
preceding day of the study because of the influence of these substances
on lipid metabolism, and to refrain from eating after 2100 h.
After an overnight fast (12 h), a cubital vein was catheterized with a
small bore extension set with a Smartsite needleless valve port
equipped with a disposable vacutainer (Vacutainer, Meylen, Cedex,
France). A baseline fasting blood sample (14 mL) was then collected
into 7-mL precooled vacutainer tubes (1 g/L
EDTA-K3) (0900 h). The subjects consumed the meal
within 
15 min. Immediately after the meal, blood samples (14 mL)
were drawn hourly during a 7-h postprandial period (between 0915 and
1515 h). During the period of the study, the subjects were allowed
to drink water and undertook only light activities.
Blood samples were placed into ice water and plasma recovered rapidly
by centrifugation (1750 x g, 20 min, 1°C). NaAzide,
phenylmethylsulfonyl fluoride and aprotinin were added to the plasma to
a final concentration of 1 mmol/L, 10 µmol/L and 28 mg/L,
respectively (22)
. Plasma was kept at 4°C for 12 h
until lipoprotein fractionation.
Isolation of TRL.
TRL [(Sf) > 400 fraction, d (kg/L) > 0.93]
were isolated from 4 mL of plasma layered with 6 mL of a NaCl solution
(d = 1.006 kg/L) by a single ultracentrifugation spin
(95000 x g, 42 min, 15°C) (23
,24)
.
Ultracentrifugation was performed using a SW 41 Ti rotor in a Beckman
L8–70M preparative ultracentrifuge (Beckman Instruments, Palo Alto,
CA). TAG concentrations were measured in plasma and in the TRL fraction
(Sf > 400) in the control and test samples by a colorimetric
enzymatic method (Peridocrom Triglycerides GPO-PAP kit, Boehringer
Mannheim, Mannheim, Germany).
Identification of apolipoproteins in the TRL fraction.
The structural apo B-100 and B-48 were taken as an indicator of the
presence of VLDL and chylomicrons, respectively, in the isolated TRL
fraction. TRL were isolated at 2 and 6 h as above from plasma
containing benzamidine (0.03%) to prevent scission of apo B. Apo B-100
and B-48 were identified by the Laemmli SDS-PAGE system (7.5%
SDS-PAGE slab gels, 1.5 mm thick). The gel electrophoresis was
carried out at 30 mA/gel for 120 min (19)
.
Perfect Protein Markers (MW 10–225 kDa) (Calbiochem-Novabiochem,
Schwalbach, Germany) were used as standards, and LDL as a B-100
standard. LDL were isolated by cumulative rate centrifugation in a
density gradient using a SW 41 Ti rotor in a Beckman L8–70M
(24
,25)
.
Analysis of triacylglycerol molecular species.
TAG were vacuum-evaporated completely, redissolved in n-hexane and passed through a filter with a pore size of 0.2 µm (Millipore, Bedford, MA). The chromatographic system consisted of a model 2690 Alliance liquid chromatograph (Waters, Milford, MA), provided with a Spherisorb ODS-2 column (250 x 4.6 mm, 3-µm particle size; Waters). The liquid chromatograph was coupled to a light-scattering detector model DDL31 (Eurosep, Cergy-Pontoise, France). The system was controlled by computer through the Millenium System (Waters). The mobile phase consisted on an initial elution gradient of 20% acetone in acetonitrile; the percentage of acetone was raised to 45% in 12 min and then to 80% after 65 min, and this percentage was held until the end of the analysis. The flow rate was 1 mL/min. Quintuple analyses of 10 µL of n-hexane solution containing 0.5 g/L of pure TAG (Sigma Grade, 99% pure, Sigma Chemical, St. Louis, MO); tritridecanoin, 1,3-dioleoyl-2-palmitoyl-glycerol, trimyristin, 1,3-dioleoyl-2-stearoyl-glycerol, 1,3-dioleoyl-2-linoleoyl-glycerol, tripentadecanoin, tripalmitin, triolein and trilinolein were injected to establish the capacity factor (k') of the system.
The triacylglycerol composition was predicted by means of relationships
between the capacity factor (k') and molecular variables of the pure
TAG. We considered all of the stereospecific positions in the glycerol
molecule to be equivalent because HPLC cannot separate positional
isomers (26
,27)
. Triacylglycerols were quantified using
tridecanoin as the internal standard.
Analysis of triacylglycerol fatty acid methyl esters (FAME).
TAG were isolated by solid-phase extraction diol columns (Supelclean LC-Diol, Supelco, Bellefonte, PA) using hexane/methylene chloride (9:1, v/v) as eluent. An aliquot was taken for analysis of total fatty acids by gas-liquid chromatography (GLC). A second aliquot was stored at -80°C for further analysis of the TAG molecular species by HPLC.
TAG were transmethylated and the resulting FAME analyzed by GLC as
described by Ruiz-Gutiérrez et al. (28)
using a
model 5890 series II gas chromatograph (Hewlett-Packard, Avondale, PA)
equipped with a flame ionization detector and a capillary silica column
Supelcowax 10 (Sulpelco) 60 m in length and 0.25 mm i.d.
Analysis of triacylglycerol fatty acids in the sn-2 position.
TAG were partially hydrolyzed by pancreatic lipase (EC 3.1.1.3, Sigma
Chemical) from pigs. Hydrolysis products were separated by TLC using
silica gel 60 plates and diethylether/hexane/acetic acid (90:10:1,
v/v/v) as solvent. The monoacylglycerol band was scraped off, eluted
with hexane and treated as above for analysis of FAME
(29)
.
Statistical analysis.
Results are presented as means ± SD. The statistical
tests were performed with the GraphPAD InStat (GraphPAD Software, San
Diego, CA) and CoStat (CoHort Software, Berkeley, CA) statistical
packages. The significance of differences between the fatty acid
composition of the oils (Table 1)
, and between the oils and TRL TAG
molecular species and the fatty acid composition (Tables 3
and 4)
was
assessed by repeated-measures two-factor ANOVA. Significance of the
individual means was determined with Tukey’s post-hoc comparison
of the means. When necessary, values were transformed reciprocally
before statistical analysis to compensate for unequal variance. ANOVA
was also used to compare the profiles of TAG in plasma and in the TRL
fraction after the ingestion of the three dietary treatments (control,
VOO and HOSO) (Figs. 1
, 2)
. Differences of P < 0.05
were considered significant.
|
|
|
|
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
VOO and HOSO had equal amounts of the MUFA, oleic acid [18:1(n-9)]
(Table 1)
. VOO had a higher content of SFA and lower PUFA than HOSO.
They differed significantly in the proportions of palmitic (16:0),
palmitoleic [16:1(n-7)] and 
-linolenic [18:3(n-3)] acids, which
were higher in olive oil, and the proportions of stearic (18:0) and
linoleic [18:2(n-6)] acids, which were higher in HOSO (P
< 0.05).
Postprandial lipemic response.
After consumption of the test meals, the TAG concentration in plasma
rose from fasting levels to reach maximum postprandial levels at 2 h, and also at 6 h for VOO (Fig. 1A
). The triglyceridemic profiles in plasma after the ingestion of the two
oils did not differ. On the contrary, TAG responses in the TRL fraction
after VOO and HOSO intakes differed (P < 0.05) (Fig. 1
B). Both oils caused a biphasic trigliceridemic response,
with the TAG concentration at the 2-h peak time significantly lower
after the VOO load (P < 0.05). The presence of
TAG-TRL in blood was longer after HOSO consumption as shown by a
longer time of TAG disappearance, 5 h for HOSO vs. 4 h for
VOO. The TAG response after the control treatment differed from after
the test meals (P < 0.05).
SDS-PAGE indicated the presence of apo B-48 and apo B-100 within the TRL fraction of Sf > 400 (data not shown). Apo B-48 can serve as a marker for intestinally derived lipoproteins. Apo B-100 also could have been synthesized and secreted by the human intestine or be associated with hepatic VLDL.
Triacylglycerol (TAG) composition of oils and triacylglycerol-rich lipoproteins (TRL).
Triolein (OOO) was the major TAG found in HOSO (86% of the total
triacylglycerols), whereas OOO (62%) and palmitoyl-dioleoyl-glycerol
(POO) (29%) were the most abundant TAG present in VOO (Table 3
). The proportions of the individual molecular species present in the
lipoprotein fraction at the maximum height of the early TRL peak (2 h
after ingestion) differed from their composition in the parent oils.
The percentage of OOO decreased significantly by 20% in both groups
(P < 0.05). The intake of olive oil produced a wider
variety of saturated triacylglycerols such as tripalmitin (PPP) and
distearoyl-oleoyl-glycerol (SSO), and increased the percentage of other
minor TAG in the lipoprotein fraction. Only palmitoyl-dioleoyl-glycerol
(POO), stearoyl-dioleoyl-glycerol (SOO) and
palmitoyl-oleoyl-stearoyl-glycerol (POS) were unaffected. In contrast,
HOSO oil ingestion produced less marked changes in the lipoprotein
triacylglycerol composition, although it is important to note the
significant decrease in trilinolein (LLL) and concomitant increase in
linoleoyl-dioleoyl-glycerol (LOO) (P < 0.01).
Triacylglycerol molecular species composition along the postprandial period.
Individual TAG concentrations after control and test treatments are
shown in Figure 2
. Each TAG profile differed between the two oil treatments (P
< 0.05). The TAG concentration returned toward basal levels more
quickly after VOO than after HOSO intake. The fastest removal of the
TAG occurred from 2 to 4 h after ingestion of VOO, in comparison
with the longer time after HOSO administration, 2–5 h. This occurred
in all of the TAG identified and did not depend on the concentration of
the TAG in the particle.
Triacylglycerol fatty acid composition.
The fatty acid compositions of the TAG at the peak time (2 h) and
valley times of 4 h (VOO) and 5 h (HOSO) are presented in
Table 4
. The predominant fatty acids in the TRL fraction at the 2-h peak time
were oleic and palmitic acids after VOO treatment, but oleic and
linoleic acids after HOSO treatment. TRL after VOO treatment were
richer in palmitic, -linolenic, docosapentaenoic [22:5(n-3)] and
docosahexaenoic [22:6(n-3)] acids compared with TRL after HOSO
treatment (P < 0.05). HOSO-TRL showed higher
percentages of linoleic, stearic and arachidonic [20:4(n-6)] acids
than VOO-TRL (P < 0.05). TAG in TRL remnants
resulted in a significant decrease in oleic acid and a concomitant
increase in SFA such as myristic (14:0) and stearic acids (P
< 0.05) 4 h after ingestion of the VOO meal. The percentages
of PUFA of the (n-6) and (n-3) families were also increased
(P < 0.01). TAG in TRL remnants (5 h) after HOSO
treatment showed a significant decrease in oleic acid and an increase
in palmitic acid (P < 0.05); PUFA of the (n-3) family
increased at a lower rate than in TRL after VOO treatment (P
< 0.05).
Positional distribution of fatty acids in TRL-triacylglycerols.
The sn-2 fatty acids in the glycerol backbone 2 h after
olive oil ingestion included palmitic, stearic, oleic and linoleic
acids as the main constituents (Table 5
). Triacylglycerols derived from HOSO ingestion presented the same fatty
acid composition but with significantly more SFA (palmitic and stearic
acids) and less oleic acid (P < 0.05) esterified to
the sn-2 position.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
17
18)
. This suggests that factors other than the oleic
acid content may be responsible for the different metabolic effects in
the fasting state. The aim of this study was to evaluate in detail
whether two oils with equal amounts of MUFA (oleic acid) but different
compositions of minor fatty acids and TAG molecular species could
produce different TRL responses in the postprandial state. This was
achieved by comparing the TAG molecular species present in the TRL
fraction after the ingestion of either VOO or HOSO by healthy men
during a 7-h postprandial period. In this study, VOO intake reduced the
postprandial TAG lipoprotein response. Lower percentages of stearic and
palmitic acids and a higher proportion of oleic acid were in the
sn-2 position of the TAG-TRL derived from VOO. The
findings indicate that the oleic acid content in a MUFA-rich oil
does not seem to be the main factor affecting postprandial TAG
metabolism. Rather, we contend that other minor fatty acids (stearic,
linoleic acids) and their positional distribution into TAG may be of
major physiologic relevance in adult normolipidemic subjects.
There is epidemiologic evidence for a role of plasma TAG in
atherosclerosis; most studies show a positive correlation between TAG
levels and the risk for cardiovascular disease (30)
. In
our study, the TAG profiles in plasma and TRL clearly demonstrated that
two oils with similar MUFA composition can produce equal TAG plasma
concentrations but different TAG-TRL responses during the
postprandial period. Even though VOO and HOSO were supplemented
equally, the concentration of TAG in TRL after HOSO intake was
significantly higher and remained in blood longer than after VOO
ingestion during the early postprandial period. Therefore, the
determination of total plasma TAG levels can be misleading when
studying the effects of dietary oils in the postprandial period if the
TAG-TRL fraction is not considered.
The major emphasis of our study was to investigate the TAG molecular species present in postprandial TRL after the ingestion of VOO and HOSO. TRL had a better balanced TAG composition compared with the dietary oils. It is important to note that dioleoyl-linoleoyl-glycerol, which is a small component of both oils, became a major component in TRL. The reason is unknown but it could be a mechanism for supplying the tissues with the essential fatty acid, linoleic acid.
We detected a different metabolic processing of TAG-TRL
derived from VOO and HOSO, as indicated by their different TAG patterns
during the postprandial period. The TAG molecular species returned
toward basal levels more slowly after HOSO intake; this may have been
due to a slow rate of clearance of TAG and/or a greater formation of
TRL after HOSO ingestion. In this respect, the high concentration of
linoleic acid in HOSO could have increased the transport of TAG into
the enterocyte, resulting in a greater secretion of chylomicrons
(31)
. Other minor nonfatty acid constituents in the oils,
such as sterols, may account for some of the differences in plasma
lipid concentrations observed after consumption of diets similar in
fatty acid content (32)
. The mechanisms involved are the
inhibition of cholesterol absorption in the small intestine and/or
increased biliary excretion (33
,34)
. A cholesterol
absorption diminished by the presence of sterols could result in an
attenuated formation of chylomicrons in the enterocyte. We contend that
the sterols present in the oils in this study did not affect the
formation of TRL because the concentration of TRL after HOSO ingestion
was greater than after VOO intake, even though HOSO contain a greater
total amount of sterols than VOO (15)
. In agreement with
our hypothesis, plasma TAG levels have been found not to be affected by
plant sterols (35)
.
We did find differences in the stereospecific fatty acid location
in the lipoprotein TAG. TAG-TRL derived from HOSO ingestion had a
lower percentage of oleic acid and were enriched in stearic and
palmitic acids in the sn-2 position compared with
TAG-TRL after VOO intake. These structural differences may have
been responsible for the slower clearance of HOSO remnant particles
because stearate in the 2-position retards the uptake of chylomicron
remnants by the liver (12)
. The susceptibility of the TAG
to hydrolysis by LPL, which is also involved in TAG clearance, does not
seem to be affected by the position to which fatty acids are esterified
to the glycerol backbone (36)
. In disagreement with our
results, Summers et al. (37)
suggested recently that
the metabolic events after LPL-hydrolysis of chylomicron-TAG
are largely unaffected by the nature or the position of stearic and
oleic acids within dietary TAG. However, the authors showed maximal TAG
response in plasma and TRL at 4 and 5 h after ingestion, which is
later than the normal diurnal pattern in which the maximal
triacylglycerol response occurs after 2–3 h (38
,39)
. It
is therefore likely that some metabolic processes from digestion to
lipid transport could have been affected, not excluding the possibility
of an impairment in the clearance of TRL-remnants through hepatic
receptor saturation (40
,41)
.
The ingestion of VOO significantly increased the content of
long-chain (n-3) PUFA (docosapentaenoic and docosahexaenoic acids)
in TAG of TRL compared with HOSO intake. We also detected an
accumulation of (n-3) PUFA in the VOO chylomicron remnant particles,
possibly due to ester bond resistance of these fatty acids to LPL
action. Intestinally derived remnant lipoproteins are taken up by the
liver (42)
; therefore, an enrichment of (n-3) PUFA in the
VOO chylomicron remnants would imply a better availability of these
fatty acids for VLDL formation. This is consistent with our previous
findings in which VOO, but not HOSO promoted the presence of
docosahexaenoic and docosapentaenoic acids in TAG of VLDL from healthy
subjects (14)
and patients with untreated essential
hypertension (43)
and corroborates our previous hypothesis
that the availability of (n-3) PUFA for the resynthesis of TAG-VLDL
in the liver may be increased by the consumption of VOO. This is of
major metabolic importance because (n-3) PUFA competitively inhibit the
utilization of arachidonic acid by the cyclooxygenase pathway and
subsequent output of eicosanoids (44
,45)
.
In conclusion, this study shows that VOO intake results in lower postprandial TAG-TRL concentration than after HOSO intake. All of the TAG molecular species identified returned toward basal levels more quickly after VOO compared with HOSO intake. Our findings suggests that the oleic acid concentration in a MUFA-rich oil may not itself be the main factor affecting postprandial triacylglycerol metabolism. We hypothesize that other minor fatty acids such as linoleic acid and the 2-positional distribution of saturated fatty acids (stearic, palmitic acids) into the TAG molecule may be of physiologic relevance.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
3 Abbreviations used: apo, apolipoprotein; FAME,
fatty acid methyl esters; GLC, gas-liquid chromatography; HOSO,
high oleic sunflower oil; LLL, trilinolein; LOO,
linoleoyl-dioleoyl-glycerol; LPL, lipoprotein lipase; MUFA,
monounsaturated fatty acids; OOO, triolein; POO,
palmitoyl-dioleoyl-glycerol; POS, palmitoyl-oleoyl-stearoyl-glycerol;
PPP, tripalmitin; PUFA, polyunsaturated fatty acids; Sf, svedberg
flotation rate; SFA, saturated fatty acids; SOO,
stearoyl-dioleoyl-glycerol; SSO, distearoyl-oleoyl-glycerol; TAG,
triacylglycerol; TRL, triacylglycerol-rich lipoprotein; VOO, virgin
olive oil.
Manuscript received June 26, 2000. Initial review completed August 23, 2000. Revision accepted October 17, 2000.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Karpe F., Steiner G., Uffelman U. Postprandial lipoproteins and progression of coronary atherosclerosis. Atherosclerosis 1994;106:83-97[Medline]
2. Karpe F., Hamsten A. Postprandial lipoprotein metabolism and atherosclerosis. Curr. Opin. Lipidol. 1995;6:123-129[Medline]
3.
Groot P. H., van Stiphout W. A., Krauss X. H. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler. Thromb. 1991;11:653-662
4. Simpson H. S., Williamson C. M., Olivecrona T. Postprandial lipemia, fenofibrate and coronary artery disease. Atherosclerosis 1990;85:193-202[Medline]
5. Lewis G. F., Steiner G. Hypertriglyceridemia and its metabolic consequences as a risk factor for atherosclerotic cardiovascular disease in non-insulin-dependent diabetes mellitus. Diabetes Metab. Rev 1996;12:37-56[Medline]
6. Roche H. M., Zampelas A., Knapper J.M.E. Effect of long-term olive oil dietary intervention on postprandial triacylglycerol and factor VII metabolism. Am. J. Clin. Nutr. 1998;68:552-560[Abstract]
7. Roche H. M., Zampelas A., Jackson K. G., Williams C. M., Gibney M. J. The effect of test meal monounsaturated fatty acid:saturated fatty acid ratio on postprandial lipid metabolism. Br. J. Nutr. 1998;79:419-424[Medline]
8.
Dugi K. A., Dichek H. L., Santamarina-Fojo S. Human hepatic and lipoprotein lipase: the loop covering the catalytic site mediates lipase substrate specificity. J. Biol. Chem. 1995;270:25396-25401
9. Huff M. W., Miller D. B., Wolfe B. M., Connelly P. W., Sawyez C. G. Uptake of hypertriglyceridemic very low density lipoproteins and their remnants by HepG2 cells: the role of lipoprotein lipase, hepatic lipase, and cell surface proteoglycans. J. Lipid Res. 1997;38:1318-1333[Abstract]
10. Niemeir A., Gåfvels M., Heeren J., Mejer N., Angelin B., Beisiegel U. VLDL receptor mediates the uptake of human chylomicron remnants in vitro. J. Lipid Res. 1996;37:1733-1742[Abstract]
11. Reblin T., Niemeir A., Meyer N., Willnow T. E., Kronenberg F., Dieplinger H., Greten H. Cellular uptake of lipoprotein[a] by mouse embryonic fibroblasts via the LDL receptor and the LDL receptor-related protein. J. Lipid Res. 1997;38:2103-2110[Abstract]
12. Mortimer B. C., Kenrick M. A., Holthouse D. J., Stick R. V., Redgrave T. G. Plasma clearance of model lipoproteins containing saturated and polyunsaturated monoacylglycerols injected intravenously in the rat. Biochim. Biophys. Acta 1992;1127:67-73[Medline]
13. Heyden S. Polyunsaturated and monounsaturated fatty acids in the diet to prevent coronary heart disease via cholesterol reduction. Ann. Nutr. Metab. 1994;38:117-122[Medline]
14.
Ruiz-Gutiérrez V., Morgado N., Prada J. L., Perez-Jimenez F., Muriana F.J.G. Composition of human VLDL triacylglycerols after ingestion of olive oil and high oleic sunflower oil. J. Nutr. 1998;128:570-576
15. Ruiz-Gutiérrez V., Muriana F.J.G., Villar J. El aceite de oliva virgen y las enfermedades cardiovasculares. Perfil lipídico en plasma y composición lipidica de la membrana de eritrocito humano. Grasas Aceites 1998;49:9-29
16. Muriana F.J.G., Ruiz-Gutiérrez V., Guerrero A., Montilla C., León-Camacho M., Villar J. Olive oil normalizes the altered distribution of membrane cholesterol and sodium-lithium countertransport activity in erythrocyte of hypertensive patients. J. Nutr. Biochem. 1997;8:205-210
17. Muriana F.J.G., Villar J., Ruiz-Gutiérrez V. Intake of olive oil can modulate the transbilayer movement of human erythrocyte membrane cholesterol. Cell. Mol. Life Sci. 1997;53:496-500[Medline]
18. Ruiz-Gutiérrez V., Muriana F.J.G., Guerrero A., Cert A. M., Villar J. Plasma lipids, erythrocyte membrane lipids and blood pressure of hypertensive women after the ingestion of dietary oleic acid from two different sources. J. Hypertens. 1996;14:1483-1490[Medline]
19.
Abia R., Perona J. S., Pacheco Y. M., Montero E., Muriana F.J.G., Ruiz-Gutiérrez V. Postprandial triacylglycerols from dietary virgin olive oil are selectively cleared in humans. J. Nutr. 1999;129:2184-2191
20. Cohn J. S. Postprandial lipid metabolism. Curr. Opin. Lipidol. 1994;5:185-190[Medline]
21. Orth M., Walh S., Hanish M., Friedrich I., Wieland H., Luley C. Clearance of postprandial lipoproteins in normolipidemics: role of the apolipoprotein E phenotype. Biochim. Biophys. Acta 1996;1303:22-30[Medline]
22. Karpe F., Humphreys S. M, Samra J. S., Summers L. K., Frayn K. N. Clearance of lipoprotein remnant particles in adipose tissue and muscle in humans. J. Lipid Res. 1997;38:2335-2343[Abstract]
23. Berr F., Kern F. Plasma clearance of chylomicrons labeled with retinyl palmitate in healthy human subjects. J. Lipid Res. 1984;25:805-882[Abstract]
24. Mills G. L., Lane P. A., Week P. K. Isolation and purification of plasma lipoproteins. Burdon R. H. Van Knippenrbergh P. H. eds. Laboratory Techniques in Biochemistry and Molecular Biology. A Guidebook to Lipoprotein Technique 1989; Elsvier Science Publishing, Amsterdam The Netherlands
25. Redgrave T. G., Roberts D.C.K., West C. E. Separation of plasma lipoproteins by density-gradient ultracentrifugation. Anal. Biochem. 1975;65:42-49[Medline]
26. Perona J. S., Barron L.J.R., Ruiz-Gutiérrez V. Molecular prediction of rat liver triglycerides by high performance liquid chromatography. J. Liq. Chromatogr. 1998;21:1185-1197
27. Perona J. S., Barron L.J.R., Ruiz-Gutiérrez V. Determination of rat liver triglycerides by gas-liquid chromatography and reversed-phase high-performance liquid chromatography. J. Chromatogr. B. 1998;706:173-179
28. Ruiz-Gutiérrez V., Prada J. L., Pérez-Jimenez F. Determination of fatty acid and triacylglycerol composition of human very-low-density lipoproteins. J. Chromatogr. 1993;622:117-124[Medline]
29. Ruiz-Gutiérrez V., Mazuelos F. Efecto de una dieta con aceites calentados sobre la lipasa pancreatica de rata. Grasas Aceites 1985;36:105-108
30.
Austin M. A. Plasma triglyceride and coronary heart disease. Arterioscler. Thromb. 1991;11:2-14
31. Van Greevenbroek M.M.J., Voorhout W. F., Erkelens D. W., van Meer G., de Bruin T.W.A. Palmitic acid and linoleic acid metabolism in caco-2 cells: different triglyceride synthesis and lipoprotein secretion. J. Lipid Res. 1995;36:13-24[Abstract]
32.
Perez-Jimenez F., Espino A., Lopez-Segura F., Blanco J., Ruiz-Gutiérrez V., Prada J., Lopez-Miranda J., Jimenez-Perez J. Lipoprotein concentrations in normolipidemic males consuming oleic acid-rich diets from two different sources: olive oil and oleic acid-rich sunflower oil. Am. J. Clin. Nutr. 1995;62:769-765
33. Andriamiarina R., Laraki L., Pelletier X., Debry G. Effects of stigmasterol-supplemented diets on fecal neutral sterols and bile acid excretion in rats. Ann. Nutr. Metab. 1989;33:297-303[Medline]
34. Heinemann T., Kullak-Ublick G. A., Pietruck B., Von Bergmann K. Mechanisms of action of plant sterols on inhibition of cholesterol absorption. Comparison of sitosterol and sitostanol. Eur. J. Clin. Pharmacol. 1991;40:S59-S63
35.
Jones P. J., Raeini-Sarjaz M., Ntanios F. Y., Vanstone C. A., Feng J. Y., Parsons W. E. Modulation of plasma lipid levels and cholesterol kinetics by phytosterol versus phytostanol esters. J. Lipid Res. 2000;41:697-705
36. Pufal D. A., Quinlan P. T., Salter A. M. Effect of dietary triacylglycerol structure on lipoprotein metabolism: a comparison of the effects of dioleoyl-palmitoyl-glycerol in which palmitate is esterified to the 2- or 1(3)-position of the glycerol. Biochim. Biophys. Acta 1995;1258:41-48[Medline]
37.
Summers L.K.M., Fielding B. A., Herd S. L., Ilic V., Clarck M. L., Quinlan P. T., Frayn K. N. Use of structured triacylglycerols containing predominantly stearic and oleic acids to probe early events in metabolic processing of dietary fat. J. Lipid Res. 1999;40:1890-1899
38.
Cohen J. C., Noakes T. D., Spinnler-Benade A. J. Serum triglyceride responses to fatty meals: effects of meal fat content. Am. J. Clin. Nutr. 1988;47:825-827
39.
Dubois C., Armand M., Azaisbraesco V., Portugal H., Pauli A. M., Bernard P. M., Latge C., Lafont H., Borel P., Lairon D. Effects of moderate amounts of emulsified dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults. Am. J. Clin. Nutr. 1994;60:374-382
40. Cohn J. S., McNamara J. R., Cohn S. D., Ordovas S. D., Schaefer E. J. Postprandial plasma lipoprotein changes in human subjects of different ages. J. Lipid Res. 1988;29:469-479[Abstract]
41. Havel R. J. Postprandial hyperlipidemia and remnant lipoproteins. Curr. Opin. Lipidol. 1994;5:102-109[Medline]
42. Cooper A. D. Hepatic uptake of chylomicrons remnants. J. Lipid Res. 1997;38:2173-2192[Abstract]
43. Ruiz-Gutiérrez V., Perona J. S., Pacheco Y. M., Muriana F.J.G., Villar J. Incorporation of dietary triacylglycerols from olive oil and high-oleic sunflower oil into VLDL triacylglycerols of hypertensive patients. Eur. J. Clin. Nutr. 1999;53:687-693[Medline]
44. James W.P.T. Nutritional disorders affecting the heart. Julian D. G. Gamm A. M. Fox K. M. Hall R.J.C. Poole-Wilsor P. A. eds. Diseases of the Heart 1996 W. B. Saunders London, UK.
45. Kinsella J. E. Alpha-linolenic acid: functions and effects on linoleic acid metabolism and eicosanoid-mediated reactions. Adv. Food Nutr. Res. 1994;35:2-160
This article has been cited by other articles:
|
|
 |
|
  M. Foltz, J. Maljaars, E. A. H. Schuring, R. J. P. van der Wal, T. Boer, G. S. M. Duchateau, H. P. F. Peters, F. Stellaard, and A. A. Masclee Intragastric layering of lipids delays lipid absorption and increases plasma CCK but has minor effects on gastric emptying and appetite Am J Physiol Gastrointest Liver Physiol, May 1, 2009; 296(5): G982 - G991. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lopez, B. Bermudez, Y. M. Pacheco, G. Lopez-Lluch, W. Moreda, J. Villar, R. Abia, and F. J. G. Muriana Dietary Oleic and Palmitic Acids Modulate the Ratio of Triacylglycerols to Cholesterol in Postprandial Triacylglycerol-Rich Lipoproteins in Men and Cell Viability and Cycling in Human Monocytes J. Nutr., September 1, 2007; 137(9): 1999 - 2005. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Cabello-Moruno, J. S. Perona, J. Osada, M. Garcia, and V. Ruiz-Gutierrez Modifications in Postprandial Triglyceride-Rich Lipoprotein Composition and Size after the Intake of Pomace Olive Oil J. Am. Coll. Nutr., February 1, 2007; 26(1): 24 - 31. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Perona, J. Martinez-Gonzalez, J. M. Sanchez-Dominguez, L. Badimon, and V. Ruiz-Gutierrez The Unsaponifiable Fraction of Virgin Olive Oil in Chylomicrons from Men Improves the Balance between Vasoprotective and Prothrombotic Factors Released by Endothelial Cells J. Nutr., December 1, 2004; 134(12): 3284 - 3289. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Metzler, R. Abia, M. Ahmad, F. Wernig, O. Pachinger, Y. Hu, and Q. Xu Activation of Heat Shock Transcription Factor 1 in Atherosclerosis Am. J. Pathol., May 1, 2003; 162(5): 1669 - 1676. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. J. Tittelbach and R. D. Mattes Oral Stimulation Influences Postprandial Triacylglycerol Concentrations in Humans: Nutrient Specificity J. Am. Coll. Nutr., October 1, 2001; 20(5): 485 - 493. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
