Oleic acid-rich olive vs. sunflower oil for heart health

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Hi All,

Olive oil seems beneficial relative to sunflower oil for heart health in the

pdf-available below.

Effects of Oleic Acid Rich Oils on Aorta Lipids and Lipoprotein Lipase Activity

of

Spontaneously Hypertensive Rats

S. Perona, lía Rodríguez-Rodríguez, and Valentina Ruiz-Gutierrez

http://dx.doi.org/10.1021/jf051375c

J. Agric. Food Chem., ASAP Article 10.1021/jf051375c S0021-8561(05)01375-0

Web Release Date: August 11, 2005

Abstract:

Hypertension development in the spontaneously hypertensive rat (SHR) leads to

vascular wall widening by smooth muscle cell proliferation. In these cells,

triglycerides (TG) and cholesteryl esters (CE) can accumulate until they become

foam

cells. We administrated two oleic rich oils, virgin olive (VOO) and high oleic

sunflower oils (HOSO), to Wistar-Kyoto rats (WKY) and SHR because these oils

have

been reported to reduce the risk for coronary heart disease in hypertensive

patients

and SHR. After 12 weeks of feeding, we analyzed the TG and CE composition and

the

lipolytic (lipoprotein lipase, LPL, and non-LPL) activity in aortas of these

animals. HOSO increased the content of linoleic acid in CE and TG of aortas from

both WKY and SHR as compared with animals fed VOO by proportionally decreasing

the

content of oleic acid. Conversely, VOO reduced the LPL and non-LPL lipolytic

activities, hence limiting the free fatty acids available for the synthesis of

TG

and CE in the vascular wall.

Abbreviations used: SHR, spontaneously hypertensive rat; WKY, Wistar-Kyoto rat;

TG,

triglyceride; CE, cholesteryl ester; VOO, virgin olive oil; HOSO, high-oleic

sunflower oil; BD, baseline diet; LPL, lipoprotein lipase; EL, endothelial

lipase;

LAL, lysosomal acid lipase; ACAT, acyl CoA:cholesterol acyltransferase; SFA,

saturated fatty acids; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated

fatty acids.

.... Results

CE Fatty Acid Composition.

The intake of diets rich in oleic acid (18:1, n-9) was reflected in aorta CE

(Table

4). The concentration of this fatty acid was higher in rats fed VOO or HOSO than

in

the groups fed BD (p < 0.05), accounting for about 60% of total fatty acids and

representing a good marker of consumption of oleic acid rich oils. In contrast,

the

content of another MUFA, palmitoleic acid (16:1, n-7), was lower in animals

receiving the oleic acid rich oils (p < 0.05). The concentration of this fatty

acid

was lower in the hypertensive animals fed the high oleic diets (p < 0.05). The

BD

was responsible for a higher accumulation of saturated fatty acids (SFA) in the

aortas of the both normo and hypertensive rats, mostly due to accumulations of

palmitic (16:0) and stearic (18:0) acids. The latter was also found in higher

concentration in animals fed HOSO. The content of linoleic acid (18:2, n-6) was

likewise significantly higher in the aortas of the rats fed BD (p < 0.05). The

content of this fatty acid in CE from aorta of rats fed VOO was much lower than

in

those fed the other diets.

Very little differences were found among groups due to hypertension. Stearic

acid

was lower in SHR rats fed HOSO or VOO as compared to the corresponding WKY (p <

0.05). Linoleic acid was in higher concentration in the SHR animals fed HOSO

than in

the control ones (p < 0.05).

TG Fatty Acid Composition.

Consumption of oleic acid rich diets was also reflected in aorta TG (Table 3).

The

content of this fatty acid was about 50% in TG form aortas of WKY animals fed

VOO or

HOSO. However, whereas in SHR rats the concentration was reduced to 37% when

HOSO

was administrated, no differences were observed as compared to WKY after VOO.

The BD was responsible for a greater amount of stearic and palmitic acids. No

differences were observed among WKY rats fed VOO or HOSO for stearic acid, but

the

content of palmitic acid in SHR fed VOO was higher than in those fed HOSO. The

concentrations of linoleic acid were higher in the TG of the rats after the

administration of HOSO (p < 0.05). VOO consumption caused a reduction in the

content

of this fatty acid in SHR rats (p < 0.05) but not when the animals were fed BD

or

HOSO.

TG Molecular Species Composition.

The diets enriched in oleic acid provided molecular species of TG rich in that

fatty

acid to the aortas of SHR and WKY rats (Table 5). The main species were

palmitoyl-diloleoyl-glycerol (POO) and triolein (OOO) accounting for more than

45%

in both groups of animals. Actually, dioleoyl-acyl-glycerol species accounted

for

more than 60% of total TG species. In contrast, BD-fed rats had significantly

higher

amounts of TG rich in SFAs, such as myristic, palmitic, and stearic acids (p <

0.05). It is interesting to note that more than 20% of TG contained myristic

acid in

WKY and SHR rats fed BD whereas in VOO- and HOSO-fed rats it was only about 11%.

Rats fed HOSO contained higher amounts of linoleic acid rich species (p < 0.05).

Oleoyl-dilinoleoyl-glycerol (OLL), dioleoyl-linoleoyl-glycerol (OOL), and

palmitoyl-oleoyl-linoleoyl-glycerol (POL) were found in higher concentrations in

aortas of rats fed HOSO than in the ones fed VOO (p < 0.05). The content OOO was

lower in hypertensive rats after the intake of both oleic acid rich oils as

compared

with the WKY animals (p < 0.05). However, this effect was not observed for the

other

dioleoyl-acyl-glycerol species in which the other fatty acid was saturated

[mytistoyl-dioleoyl-glycerol (MOO) and palmitoyl-dioleoyl-glycerol (POO)].

Differences in the content of other oleic acid-containing TG were found between

SHR

and WKY animals. OOL was lower and dipalmitoyl-oleoyl-glycerol (PPO) was higher

in

SHR rats fed VOO, and palmitoyl-stearoyl-oleoyl-glycerol (PSO) was lower and

stearoyl-dioleoyl-glycerol (SOO) higher in hypertensive animals fed HOSO (p <

0.05).

Lipolytic Activity.

LPL activity was increased very importantly in SHR rats fed the BD diet as

compared

to WKY (p < 0.05). However, this effect was not observed in animals fed VOO or

HOSO.

In the latter groups, the LPL activity of the SHR rats was lower than in the

control

equivalents, although only for HOSO the difference was significant (p < 0.05).

Hypertension also caused the increment of non-LPL lipolytic activity in animals

fed

the BD (p < 0.05). However, for this activity, the decrease observed after

consuming

the oleic acid rich oils was not significant. VOO increased non-LPL lipolytic

activity in aortas of normotensive animals as compared with the other dietary

groups

(p < 0.05) and in hypertensives as compared with the HOSO group (p < 0.05).

Discussion

Adult SHR present cardiac hypertrophy and increased proliferation of smooth

muscle

cells in aorta, as well as altered LPL activity (4, 5). We administered two MUFA

rich oils to WKY and SHR because these oils have been reported to reduce the

risk

for coronary heart disease by producing similar effects on the atherogenic

parameters of hypertensive patients (26) and SHR (27). The CE composition of the

aorta showed a good compliance of the diets as the oleic acid content in the

aortas

of the animals fed VOO or HOSO was about 50% higher. Murakami et al. (32, 33)

reported increased accumulation of CEs in smooth muscle cells and macrophages

from

SHR than WKY in response to altered LDL, which was attributed to enhanced

scavenger

receptor activity and intracellular acyl CoA:cholesterol acyltransferase (ACAT)

activity. CE comprise the principal lipid class that accumulates within

macrophages

and smooth muscle cells of the atherosclerotic lesion (34).

Increased CE accumulation in vascular cells of SHR is in agreement with our

previous

results in whole aorta (35). In that study, SHR had higher CE accumulation in

rat

aorta when fed BD. VOO did not exert any effect on the accumulation of this

lipid

class in either WKY or SHR but administration of HOSO reduced CE accumulation

from

0.50 to 0.11%. In the present study, we found very little differences in the

fatty

acid composition of aorta CE caused by hypertension (Table 3). Consequently, the

accumulation of CE appears to be nonselective. VOO reduced the content of

linoleic

acid in CE of aortas from both WKY and SHR as compared with animals fed HOSO by

proportionally increasing the content of oleic acid. Additionally, BD increased

the

content of palmitic acid. Lee and Carr (36) have recently shown that dietary

palmitic acid increases the activity of ACAT in the liver of Syrian hamsters

leading

to increased accumulation of CE in apo B-100 lipoproteins. Although these and

other

authors did not find any difference on ACAT activity between dietary oleic and

linoleic acids, others have suggested that linoleic acid may, in fact, inhibit

ACAT

activity (37). Unfortunately, there is very scarce information on the influence

of

free fatty acids on CE accumulation and/or ACAT activity in smooth muscle cells.

Therefore, these results indicate that BD increases CE accumulation in aortas of

SHR

by increasing the incorporation of palmitic acid into this lipid class by ACAT.

For

the same reason, HOSO consumption might reduce CE accumulation in smooth muscle

cells by providing more linoleic acid. However, it cannot be discarded that the

lower content on linoleic acid in CE of smooth muscle cells is related to its

higher

oxidizability.

TGs also accumulate in the atherosclerotic plaque, giving to smooth muscle cells

the

aspect of foam cells, just like macrophages (34). In our study, TGs from rat

aorta

fed HOSO were enriched in linoleic acid, whereas rats fed VOO were enriched in

oleic

acid (Table 4). The consequence was a higher accumulation of linoleic acid rich

TG

species (OLL, OOL, and POL) in aortas of the HOSO group as compared with the VOO

group, although the content in OOO and POO was similar for both dietary groups

(Table 5). In our earlier study, we found increased TG accumulation in SHR

animals

after consumption of HOSO as compared with VOO (35). With our present results,

we

can suggest that such TG accumulation occurring in hypertensive animals was due

mainly to increased linoleic acid rich species. The presence of one double bond

in

the molecule makes linoleic acid more susceptible to oxidation than oleic acid,

and

it is well-known that oxidation products from linoleic acid are responsible for

the

deterioration of the vascular endothelium (38, 39).

The income of fatty acids into the vascular wall may be due to two main

pathways:

direct receptor-mediated lipoprotein uptake and lipoprotein hydrolysis by LPL.

LPL

is a TG hydrolase, acting mainly on TG rich lipoproteins (TRL), whereas EL is a

phospholipase acting mainly on HDL, hence releasing high amounts of free fatty

acids

(9). In the present study, hypertension increased LPL activity in SHR fed the BD

(Figure 1). A negative relationship between the development of hypertension in

SHR

and the cardiac LPL activity has been found (7, 40). Shepherd et al. (40) also

found

a reduced vascular endothelial-bound LPL activity in SHR. However, in that

study,

they reported increased LPL activity in SHR diabetic rats. Actually, treatment

of

these rats with insulin for 2 weeks prevented the increase. It is therefore

tempting

to speculate that since SHR are known to be insulin resistant (41), when on a

long

term, low fat, high carbohydrate diet, SHR may behave as diabetics. The

consequence

of enhanced LPL activity implies more free fatty acids available for TG and CE

synthesis, which is concordant with the increased accumulation of these lipid

classes observed in our previous report (35). Although we did not measure EL

activity here, this enzyme could contribute to the fatty acid influx to aortas

of

SHR. Shimokawa et al. (42) have very recently shown increased mRNA expression

for EL

in aortas of SHR, which they related to a decrease in plasma HDL in these

animals.

--------------------------------------------------------------------------------

Figure 1 LPL activity in the aortas of WKY and SHR fed the BD and the diets

enriched in VOO or HOSO. For the letters a-c, mean values within a row sharing

the

same letter are not significantly different (P < 0.05).

Figure 2 Non-LPL activity in the aortas of WKY and SHR fed the BD and the diets

enriched in VOO or HOSO. For the letters a and b, mean values within a row

sharing

the same letter are not significantly different (P < 0.05).

--------------------------------------------------------------------------------

Conversely, when SHR were fed high fat diets, we found the reduced LPL activity

due

to hypertension reported before (40), although it was only statistically

significant

after HOSO but not after VOO. The consequence of lower LPL activity in the

aortic

wall would lower lipoprotein hydrolysis and fatty acid incorporation to vascular

cells. At the same time, a lower expression of the VLDL receptor has been found

in

cardiac cells of SHR (43). Hence, the higher TG accumulation found in aortas of

SHR

fed HOSO would be due to higher fatty acid incorporation into cells but to

decreased

TG hydrolysis. This would be in agreement with the lower non-LPL lipolytic

activity

shown in the present study, which might be due to a lower preference of the

hydrolytic enzymes for linoleic acid-containing lipid classes. A lower LPL

activity

in SHR fed HOSO as compared to VOO had been observed before in adipose tissue,

which

was also concomitant to increased TG molecular species containing linoleic acid,

mainly OOL (28). However, in the heart, we could not find any relevant effect of

diets enriched in HOSO or VOO on the LPL activity in these hypertensive animals

(29).

Free fatty acids released in blood vessels by enzymes attached to the vascular

endothelium may injury arterial wall cells (16, 17). They can induce foam cell

formation in macrophages (18) and TG accumulation in smooth muscle cells (19).

Lysosome acid lipase (LAL), which can hydrolyze CE and TG, seems to be the only

lipolytic enzyme within these cells, since no other TG-hydrolase has been found

(36). During the progression of the atherosclerotic plaque, a reduction in the

content of TG occurs, whereas the amount of CE is increased. Consequently, this

process may be affected by the hydrolytic action on TG molecular species. The

rate

of hydrolysis might depend on the TG fatty acid composition, just as occurs in

other

tissues (44, 45).

In conclusion, the results shown in the present study indicate that VOO would

help

to normalize the lipid composition of the aortic wall of SHR by maintaining the

LPL

and non-LPL lipolytic activity closer to the levels of healthy WKY. However, we

also

report now that the reduction of the CE content in the aorta of SHR reported

before

(35) was mediated by a lower incorporation of linoleic acid, probably due to

reduced

ACAT activity. The fate of this fatty acid was, in turn, TG synthesis, which

would

explain the higher concentration found in our previous study. Because TGs are

more

readily hydrolyzed than CE, HOSO would also help to reduce the conversion of

smooth

muscle cells into foam cells in SHR.

Al Pater, PhD; email: old542000@...

____________________________________________________

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