Access to this full-text is provided by Wiley.
Content available from Disease Markers
This content is subject to copyright. Terms and conditions apply.
Research Article
Avocado Oil Supplementation Modifies Cardiovascular
Risk Profile Markers in a Rat Model of Sucrose-Induced
Metabolic Changes
Octavio Carvajal-Zarrabal,1Cirilo Nolasco-Hipolito,2
M. Guadalupe Aguilar-Uscanga,3Guadalupe Melo-Santiesteban,4
Patricia M. Hayward-Jones,1and Dulce M. Barradas-Dermitz5
1Biochemical and Nutrition Chemistry Area, University of Veracruz, SS Juan Pablo II s/n, 94294 Boca del R´
ıo, Ver., Mexico
2Department of Molecular Biology, Faculty of Resource Science and Technology, University Malaysia Sarawak,
94300 Kota Samarahan, Sarawak, Malaysia
3Food Research and Development Unit, Veracruz Institute of Technology, Calz. M.A. de Quevedo 2779, 91860 Veracruz, Ver., Mexico
4Pathology Laboratory, Institute of Forensic Medicine, University of Veracruz, SS Juan Pablo II s/n, 94294 Boca del R´
ıo, Ver., Mexico
5Biological-Chemistry Area, Veracruz Institute of Technology, Calz. M.A. de Quevedo 2779, 91860 Veracruz, Ver., Mexico
Correspondence should be addressed to Octavio Carvajal-Zarrabal; ocarvajal@uv.mx
Received June ; Revised December ; Accepted December ; Published February
Academic Editor: Fabrizia Bamonti
Copyright © Octavio Carvajal-Zarrabal et al. is is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
e purpose of this study was to evaluate the eects of avocado oil administration on biochemical markers of cardiovascular risk
prole in rats with metabolic changes induced by sucrose ingestion. Twenty-ve rats were divided into ve groups: a control group
(CG; basic diet), a sick group (MC; basic diet plus % sucrose solution), and three other groups (MCao, MCac, and MCas; basic
diet plus % sucrose solution plus olive oil and avocado oil extracted by centrifugation or using solvent, resp.). Glucose, total
cholesterol, triglycerides, phospholipids, low- and high-density lipoproteins (LDL, HDL), very low-density lipoprotein (VLDL),
lactic dehydrogenase, creatine kinase, and high sensitivity C-reactive protein concentration were analyzed. Avocado oil reduces
TG, VLDL, and LDL levels, in the LDL case signicantly so, without aecting HDL levels. An eect was exhibited by avocado oil
similar to olive oil, with no signicant dierence between avocado oil extracted either by centrifugation or solvent in myocardial
injury biochemical indicators. Avocado oil decreased hs-CRP levels, indicating that inammatory processes were partially reversed.
ese ndings suggested that avocado oil supplementation has a positive health outcome because it reduces inammatory events
and produces positive changes in the biochemical indicators studied, related to the development of metabolic syndrome.
1. Introduction
Food is a factor that plays a key role in life style, a determining
inuence on health and quality of life. It is known that popula-
tions with a high consumption of meat, dairy foods, and sugar
have a higher mortality rate than those that feed mainly on
fruits, vegetables, sh, and unsaturated oils []. Undesirable
eectsonhealthareassociatedwithanexcessiveintake
of carbohydrates (sugars) and fats. Manifestations of health
disorders in people with metabolic implications are related
to the incidence and prevalence of chronic and degenerative
diseases such as obesity, diabetes, cardiovascular disease, and
dyslipidemia (low HDL-cholesterol and high triglycerides),
among others [,]. Although there are many factors that
contribute to its development, one of the main causes that
lead to these conditions is the diet that is consumed. A diet
containing a great amount of nutrients produces a strong
impact on structure, physiology, and cellular metabolism.
In recent years, the increase in these diseases has become a
global public health problem inspite of the increasing medical
knowledge for their prevention and treatment; consequently,
the nutritional aspect seems to remain vital.
Hindawi Publishing Corporation
Disease Markers
Volume 2014, Article ID 386425, 8 pages
http://dx.doi.org/10.1155/2014/386425
Disease Markers
Statistics from the Secretary of Health in Mexico indicate
that the incidence of cardiovascular diseases has increased
in recent years, so that now they are the leading cause of
death worldwide (WHO, ). On the other hand, reports
found in scientic literature about the health benets of
the Mediterranean diet and olive oil have attracted interest
in research on the eects and consumption of oils rich in
monounsaturated fatty acids, particularly oleic acid, and its
relationship with metabolic syndrome, which predisposes the
individual to more serious complications, such as diabetes
and cardiovascular diseases [–].
Mexico is a major world producer of avocados; this
fruit is a rich potential source of oil (– g/ g of fruit),
mostly monounsaturated [], and a good source of linoleic
acid []. It also contains high levels of antioxidants including
polyphenols, proanthocyanidins, tocopherols, and caroten-
oids which have shown positive health outcomes. It has also
been established that soluble components of avocado oil
confer these antioxidant properties. Studies in human and
animal models have shown that this oil helps to control
weight, reduces the risk of diabetes [], normalizes blood
cholesterol levels [], is involved in liver metabolism [], and
helpsinskincare[]. Other studies reported the presence
of functional molecules such as glutathione [], a molecule
related to decreased risk of cancer. On the other hand, the
unsaponiable components, rich in antioxidant molecules
[], have also shown benecial eects on anti-inammatory
processes related to the development of cancer [].
In the relevant literature, the benets generated by
including olive oil in the diet for cardiovascular disease risk
reduction are well documented. Due to similarities in lipid
composition between olive oil and avocado oil, it may be
assumed that the high concentration of monounsaturated
fattyacidsinavocadooilcouldbeasadequateasoliveoilfor
lowering blood lipid levels. In addition, the phytochemical
components of avocado oil are also related to the disease
manifestations associated with an altered metabolic prole;
so overall, it is expected that all the benecial properties of
avocado oil will achieve positive health eects.
2. Material and Methods
2.1. Avocado Oil Extraction. ere are dierent technologies
for extracting oil from the avocado and they can aect its
quality. e oil was obtained from Hass avocado purchased
from a local market in the Port of Veracruz, Mexico. When
edible maturity had been reached, the avocados were washed
and peeled and the seed was removed. Subsequently, the
pulp was homogenized by adding tert-butylhydroquinone
(TBHQ) at .% (w/w).
2.1.1. Oil Extraction by Centrifugation. e avocado pulp was
mixed with water to achieve a : w/v and NaCl (.%w/w),
the pH was adjusted to . with ascorbic acid, and the mixture
was homogenized in a blender (Black & Decker Model MX
) at , rpm for hour at ∘C. Subsequently, the oil
was removed by centrifugation at rpm in a tubular
continuous centrifuge (Cepa-Schnell, GLE Model NBS) fed
at . L/min.
T : Composition of basal and experimental diets formulated
according to AIN-.
Ingredients Basal diet (g)
Cornstarch .
Casein .
Cellulose .
Mineral mix AIN- .
Vitamin mix AIN- .
DL-methionine .
Tert-butylhydroquinone .
Fat†.
†Corn-canola in the basal diet (CG and MC groups); experimental diets
(MCao, MCac, and MCas resp.) were formulated with olive oil or avocado
oil, extracted either by centrifugation or solvent.
2.1.2. Avocado Oil Extraction by Solvent. Ahomogenatewas
made with a portion of the avocado pulp and two parts
of a mixture of hexane-isopropanol ( : v/v) in separate
funnels, and the oil phase was collected. Subsequently, the
solvent was removed in a rotary evaporator (Buchi R-,
Labortechnik AG, Switzerland) at ∘C and mmHg
pressure. e remaining solvent was removed by entrainment
with nitrogen gas and then the oil was exposed to high
vacuum in a freeze dryer for h. ereaer the oil was stored
in refrigeration and protected from light until use.
2.2. Experimental Animals and Diets. In this experiment
male Sprague-Dawley weaned rats ( weeks old and weighing
± g) were purchased from Teklad, Co. (Mexico City),
and caged individually in stainless steel boxes in a room
with controlled temperature (∘C) and a light-dark cycle
of hours. e experimental protocol for the management
of experimental animals was approved by the animal ethics
committee, Biochemical and Nutrition Chemistry Area, Uni-
versity of Veracruz. e basal diet was prepared according
totheAmericanInstituteofNutrition[]asshownin
Table . A mixture of corn-canola oil (.g/ g diet) was
used as a source of dietary fat (Patrona from the local
market). e experimental diet was prepared based on the
composition of the basal diet plus oil (.% w/w): olive
oil (carbonell), avocado oil extracted by centrifugation or
solvent, respectively. Diets were prepared once a week and
kept in powder form at ∘C until use. As part of this study, the
fatty acid composition of the oils used in preparing diets was
analyzed and it was found that all the oils had a rather similar
composition, mainly oleic and linoleic acids (Table ).
2.3. Sucrose-Induced Metabolic Changes Model. e animals
were divided into two groups: a control group (CG, 𝑛=5)
receiving a basal diet and a group with sucrose-induced
metabolic changes (MC, 𝑛=20), which received the basal
diet plus % sucrose solution as drinking water to induce
this condition. e animals had free access to food and water
forweeksandfoodintakewasmeasureddaily.Attheend
of this period, the diet was withdrawn for at least hours
and the manifestation of the metabolic characteristics was
Disease Markers
T : Fatty acid composition of dietary oils (%).
Fatty acid Corn Canola Olive AvocadocAvo cad os
: . . . . .
: . . . . .
: . . . . .
: . . . . .
: . . . . .
: . . . . .
Values are expressed as mean of duplicate analysis. Avocadoc:avocadooil
extracted by centrifugation; avocados: avocado oil extracted by solvent.
checked by determining body weight; then serum glucose,
triglycerides, and cholesterol levels were determined and
obtained by cardiac puncture.
2.4. Animal Treatment
2.4.1. Experimental Diet Management. Once the sucrose-
induced metabolic changes model had been obtained, the
MC animals were divided into four groups of ve rats
each. One group was maintained on the basal diet (the
sick group, MC); three groups of rats designated, as MCao,
MCac, and MCas, respectively, received an experimental
diet containing .% w/w oil (olive and avocado extracted by
centrifugation or extracted with solvent) as the sole source
of dietary fat. ese four groups received the experimental
diets and water with % sucrose solution for weeks. e
CG group continued to receive only the diet with corn-
canola oil and no sucrose in the drinking water. Diets were
prepared once a week and kept refrigerated until use. At
the end of the experiment the diet was withdrawn, and the
fasting animals were sacriced through decapitation. Serum
glucose, cholesterol, triglyceride, and phospholipid levels
were determined. All animals were sacriced and the organs
were extracted for further analysis.
2.5. Biochemical Indicators. All biochemical indicator anal-
yses were carried out on serum blood samples. Glucose
was determined with the glucose oxidase method. Total
cholesterol (TC), triglycerides (TG), phospholipids (PL), low-
and high-density lipoprotein (LDL, HDL), very low-density
lipoprotein (VLDL), lactic dehydrogenase (LDH), creatine
kinase (CK), and high sensitivity C-reactive protein (hs-CRP)
were determined by enzymatic colorimetric methods using
commercial kits obtained from Bayer and BioMerieux, using
an automated analyzer (RA XT, Bayer Technicon) and a
microplate reader to determine hs-CRP. e fatty acid prole
of vegetable oils was determined by gas chromatography
(Hewlett Packard , Palo Alto, CA.) using pentadecanoic
acid as internal standard. All chemicals used were of analyti-
cal grade.
2.6. Statistical Analysis. e data are expressed as the mean ±
standard deviation (x±SD). Statistical signicance was
determined with analysis of variance procedures, with a post
hoc Tukey multiple-range test for comparison of means (𝑃<
0.05). Data were analysed using IBMcSPSScStatistics Version
, .
T : Growth parameters, food and caloric intake, liquid con-
sumption, and biochemical markers in control (CG) and sucrose-
induced metabolic changes (MC) rats.
Variabl e s Dietary groups
CG group MC group
Initial body weight (g) 239 ± 22 242 ± 24
Final body weight (g) 445 ± 53 470 ± 38∗
Body weight gain (g) 206 ± 1.8 228 ± 2.0∗
Food intake (g/d) 26.1 ± 1.3 14.3 ± 1.1∗∗
Liquid consumption (mL/d) 46.3 ± 3.3 58.1 ± 3.4∗
Liquid consumption (mL/d/ g bw) 9.3 ± 1.4 10.5 ± 0.6
kcal equivalent in drinking water . 10.8 ± 1.7∗∗
Glucose (mg/dL) 114 ± 18 130 ± 11
Cholesterol (mg/dL) 104 ± 12 101 ± 12
Triglycerides (mg/dL) 79 ± 12 179 ± 35∗∗
Valu e s a re mea n ±SD. CG group: 𝑛=5;MCgroup:𝑛=20.∗𝑃 < 0.05;
∗∗𝑃 < 0.01.
3. Results
3.1. Metabolic Characteristics Evaluating Rats in the Control
Group and Rats with Sucrose-Induced Metabolic Changes.
Table shows growth variables, food and caloric intake,
liquid consumption and the biochemical markers assessed
in rats of the control group (CG) and those with sucrose-
induced metabolic changes (MC).
Aer weeks, a signicant increase (𝑃 < 0.05)in
nal body weight and body weight gain was observed in
the MC group as compared to the CG group, although the
food intake in rats in the CG group was signicantly higher
(𝑃 < 0.01) than in the MC group. Contrary to this, the MC
group showed a daily liquid intake signicantly higher (𝑃<
0.05) as compared with the CG group. However, when the
daily liquid intake per g in weight was compared between
CG and MC groups, this was not signicant. e caloric
equivalent produced by liquid intake was . ±. kcal in
the MC group; the CG group did not have any energy intake,
because this group received only puried drinking water.
Triglyceride levels in the MC group were signicantly greater
(𝑃 < 0.01)thanintheCGgroup;however,nosignicantly
dierent results were found in any group for either glucose or
cholesterol levels.
3.2. Eect of Dietary Oils on Metabolic Change Biochemical
Indicators. e eect of olive and avocado oils on biochem-
ical indicators in rats with metabolic changes induced by
sucrose ingestion aer the administration of experimental
diets for weeks is shown in Tab l e .
MC group triglyceride levels increased signicantly (𝑃<
0.05),atleast.timeswithrespecttotheCGgroup.On
the contrary, MCao, MCac, and MCas groups exhibited
reduced levels, although not signicant compared to MC
andnotreachingthelowerCGlevels.Asforphospholipids,
the MC group showed signicantly increased levels (𝑃<
0.05) compared to CG; however, in MCao, MCac, and MCas
groups, no signicant change was observed when compared
to MC, but their results were signicantly higher (𝑃 < 0.05)
Disease Markers
T : Glucose- and lipid-metabolic parameters 𝑥±SD (mg/dL) in rats fed diets with dierent dietary oil sources during weeks.
Variabl e s Dietary groups
CG MC MCao MCac MCas
Glucose 147 ± 41 158 ± 18 155 ± 38 145 ± 16 131 ± 21
Triglycerides 48 ± 11 181 ± 29∗145 ± 42∗145 ± 58∗133 ± 28∗
Cholesterol 95 ± 12 91 ± 9 97 ± 11 99 ± 12 104 ± 14
Phospholipids 43 ± 4 55 ± 4∗57 ± 4∗56 ± 4∗55 ± 6∗
HDL-C 18 ± 4 18 ± 3 19 ± 3 18 ± 4 20 ± 4
LDL-C 50 ± 1 69 ± 1∗∗ 50 ± 2 51 ± 1 53 ± 1∗
VLDL 10 ± 2 36 ± 6∗30 ± 10∗29 ± 11∗28 ± 6∗
Valu e s a re mea n ±SD.
Corn-canola diet (CG group, 𝑛=5); MC group: corn-canola diet plus % sucrose in drinking water (𝑛=5); MCao group: olive oil plus % sucrose in
drinking water (𝑛=5); MCac group: avocado oil extracted by centrifugation plus % sucrose in drinking water (𝑛=5); MCas group: avocado oil extracted
by solvent plus % sucrose in drinking water (𝑛=5).
∗𝑃<0.05;∗∗𝑃<0.01compared to corresponding data in CG group.
T : Prole of myocardial injury enzymes in rats fed diets with dierent dietary oil sources during weeks.
Variabl e s Dietary groups
CG MC MCao MCac MCas
Lactic dehydrogenase (U/L) 3820 ± 955 3446 ± 1214 2974 ± 2145 802 ± 598 3573 ± 1031
Creatine kinase (U/L) 822 ± 198 556 ± 71 364 ± 220 530 ± 358 658 ± 254
High sensitivity C-reactive protein (mg/dL) 1.7 ± 0.1 3.0 ± 0.2∗∗ 1.8 ± 0.2∗1.5 ± 0.1 1.5 ± 0.1
Valu e s a re mea n ±SD.
Corn-canola diet (CG group, 𝑛=5); corn-canola diet plus % sucrose in drinking water (MC group, 𝑛=5); olive oil diet plus % sucrose in drinking water
(MCao group, 𝑛=5); avocado oil diet extracted by centrifugation plus % sucrose in drinking water (MCac group, 𝑛=5); avocado oil diet extracted by
solvent plus % sucrose in drinking water (MCas group, 𝑛=5).
∗𝑃<0.05;∗∗𝑃<0.01versus corresponding data in CG group.
when compared to CG. LDL levels in MCao and MC ac groups
did not show signicant dierences with respect to CG, but
there was a very signicant increase (𝑃 < 0.01)intheMC
group, much more than the increase (𝑃 < 0.05)inthe
MCas group. VLDL in the MC group increased . times in
comparison to CG levels and no signicant decrease from
there was observed in MCao, MCac, and MCas groups, all
still signicantly higher (𝑃 < 0.05)thanCG.Signicantly
dierent results were not found for any group in the cases of
glucose, cholesterol, or high-density lipoproteins (HDL).
3.3. Eect of Dietary Oils on Myocardial Injury Indicators. e
eectofdietaryoliveandavocadooilsonmyocardialinjury
indicators in rats with metabolic changes induced by sucrose
ingestion is shown in Tab l e .
A highly signicant increase (𝑃 < 0.01) of hs-CRP serum
levels was observed in the MC group, almost double CG
values.eMCaogroupmanagedtorevertthechangein
these levels somewhat (𝑃 < 0.05), while MCac and MCas
groups completely returned to CG values. Lactic dehydroge-
nase (LDH) and creatine kinase (CK) levels did not show any
signicant dierences for any study group compared to CG;
however, in MCao, MCac, and MCas groups, CK levels did
fall below CG values.
4. Discussion
Metabolic changes are associated with a number of diseases,
including obesity, diabetes, hypertension, dyslipidemia, and
other abnormalities of importance related to their develop-
ment. ese are grouped into dierent proles, such as liver,
pancreatic, and cardiovascular functions.
Within this framework, in the present study, signicant
dierences were found for MC groups as compared to the
CGgroupinnalbodyweightandweightgain,whichwere
signicantly higher ( and %, resp.), although food intake
was signicantly lower (%). ese results are consistent
with those reported in other studies where metabolic changes
were induced by the administration of a sucrose-rich diet
in addition to an experimental diet causing changes in the
biochemical indicators measured [,]. In relation to serum
biochemical indicators associated with the development of
metabolicabnormality,itwasfoundthatglucoseandcholes-
terol concentrations in MC group rats were similar to those
intheCGgroupandnotsignicant.ReavenandChang[]
have suggested that this is due to hyperinsulinemia developed
in metabolic abnormalities which maintains normal levels
of blood glucose. TG levels were signicantly higher (%)
in MC group rats (a . fold increase). Other studies have
found similar results [,]; Piatti et al. []reportedthe
association in healthy patients between sudden TG elevation
and insulin resistance and suggested that the increase in
blood TG in vivo inhibits glucose utilization and oxidation
stimulated by insulin action in the peripheral tissues. One
waytoexplainbloodTGelevationmightbetoconsidera
possible increase in the reesterication of fatty acids from the
liverasaresultoffructosemetabolism,asreportedbyBezerra
et al. []; this monosaccharide stems from sucrose hydrolysis
Disease Markers
and in the liver, fatty acids are mainly used for the HDL and
TG synthesis, which in turn raise serum levels.
Few studies have evaluated the inuence of avocado
oil as a dietary fat on the lipid prole and lipoprotein
metabolism, specically in animal models with manifesta-
tions of metabolic disorders. is study found that the dietary
intake of olive oil and avocado oil extracted by centrifugation
or solvent exerted little or no eect on glucose, cholesterol,
and HDL levels, there being no signicant changes in the
circulating levels of these indicators for any study group.
Among the most important eects observed in this
experiment is the signicant elevation of TG levels in the
MC group, at least .-fold compared with the CG group, a
phenomenon reversed with the subsequent administration of
olive oil or avocado extracted by centrifugation or solvent.
is eect is attributed to the ingestion of a high amount
ofsucroseinthedrinkingwaterandisafeatureofthe
metabolic disorder [], since several studies demonstrate
that high carbohydrate intake is associated with increased
TG levels []. On the other hand, the MCao, MCac, and
MCas groups were able to reduce TG levels signicantly (,
,and%,resp.)comparedtotheMCgroup,although
without reaching the lower levels of the CG group. ese
data are consistent with previous ndings by Lerman-Garber
et al. [], Carranza et al. [], and L´
opez Ledesma et al.
[],whoshowedthatadietsupplementedwithavocadooil
fordaysindiabeticsubjectswithinduceddyslipidemia
decreased TG levels by , ., and .%, respectively.
In addition, the observations reported in this study add
support to those postulated by P´
oveda et al. [], which
indicate that oils rich in monounsaturated fatty acids and
micronutrientsmayhelplowerTGlevelsandreducethe
unfavorableresponseinthelipidproleobservedwith
saturated fatty acids. Phospholipids maintained a similar
percentage increase (, , and %) in the MCao, MCas, and
MCac groups, with respect to the SG group, and showed no
signicant eect on this indicator; however, their levels were
all signicantly higher, by , , and %, respectively, in
relation to the CG group. Other researchers have reported
that, although olive oil has a hypocholesterolemic eect on
theserumlipidprole[], there is some evidence to suggest
that it does not signicantly aect the prole of heart or
erythrocyte phospholipids []. On the other hand, it has
been found that avocado oil supplementation in rats increases
thephospholipidfractioninHDLasasurfacecomponent
[]; the present study shows that avocado oil, while being
a crude oil high in micronutrients, also has a signicant
percentage of monounsaturated fatty acids (:N oleic: –
%), which could explain its eect to increase phospholipid
levels.
It has been established that the consumption of olive oil
reduces cholesterol bound to LDL (LDL-C) when replacing
a source of saturated fat or one high in carbohydrates [,
].iseecthasbeendemonstratedwithoilsrichin
monounsaturated fatty acids; however, it is not exclusive to
oliveoilandisalsoproducedbyotheroilsrichinoleicacid,
such as avocado oil. is study conrmed that olive oil very
signicantly decreased (%) LDL levels in the MCao group
and that avocado oil extracted by centrifugation (MCac) or
solvent (MCas) reduced very signicantly and signicantly
theselevels,byand%,respectively,comparedwithMC
group levels.
Itiswellknownthatamongtherelevantmechanismsof
atherosclerosis pathogenesis are the oxidation of low-density
lipoproteins (LDL) in the artery walls, the proliferation of
smooth muscle cells, endothelial activation, and leucocyte
xation.
Among the studies linked to these mechanisms and to
thepresenceofoleicacidarethosewhichrelatethetypeof
fattyacidpresentintheoilsconsumedtoLDLsusceptibility
to oxidation. Parthasarathy et al. [] demonstrated that LDL
particles rich in oleic acid are markedly more resistant to
oxidative changes. is has been corroborated by Abbey et
al. [] and Reaven et al. []wherethissameparticletype
presented greater resistance to ex vitro oxidation than those
rich in linoleic acid. Moreover, Mata et al. []reportedthat
supplementation with monounsaturated fatty acids produces
a reduction in the synthesis of smooth muscle cells in
cell cultivations incubated with human serum. Studies with
endothelial cells showed that oleic acid inhibits endothelial
activation analysed through VCAM- expression (vascular
cell adhesion molecule-) []. Carluccio et al. []suggested
that oleic acid contributes to atherosclerosis prevention by
replacing the saturated fatty acids of cell membrane phospho-
lipids and by modulating the genetic expression of molecules
implicated in monocyte capture.
Basedonalltheabove,itispossibletolinktheoleicacid
present in both olive and avocado oils used in this study to
the variety of mechanisms mentioned.
On the other hand, it is possible that part of the
hypocholesterolemic eect observed is due to changes in the
metabolism of LDL lipoproteins caused by the ingestion of
avocado oil in the diet, an eect related on the one hand
to the type of fat and, on the other, to the concentration
of biologically active microcomponents acting additively or
synergistically and not simply as isolated components [].
Experimental data indicate that polyphenols from virgin
and extra virgin oils might additionally inuence lipid
metabolism,thusreducingHMG-CoAreductaseactivityand
modifying lipid values [].
e intake of olive oil (MCao) and avocado oil extracted
by centrifugation (MCac) or solvent (MCas) signicantly
decreased (, , and %, resp.) the VLDL levels when
comparedtotheSGgroup.Ontheotherhand,supplementing
a diet with avocado oil not only lowers LDL but also TG
associated with VLDL. As it appears, in comparison with
oliveoil,thecrudeavocadooilcomponentsmaybethecause
of this metabolic eect in the liver, reducing triglyceride-
rich lipoproteins biosynthesis. ese observations have been
conrmed in previous studies [,].
Metabolic changes did not aect LDH levels; although
thelevelsofthisenzymedecreased(.%)intheMCgroup,
their values were not signicantly dierent compared to
those in the CG group. In the olive oil group (MCao),
LDH levels were reduced by % ( versus U/L),
whereas in the avocado oil groups extracted by centrifugation
(MCac) or solvent (MCas), LDH levels decreased by %
and increased by %, respectively, compared with the MC
Disease Markers
group. Moreover, in all groups, the olive oil (MCao) and
avocado oil extracted by centrifugation (MCac) or solvent
(MCas) groups, LDH levels decreased by , , and .%,
respectively,incomparisonwithCGgroup,butnosignicant
eect was observed because the values of this indicator
overlapped with those in the CG group (, , and
versus U/L, resp.).
Regarding CK, it was observed that the metabolic abnor-
mality did not signicantly aect its levels. e SG group had
decreased CK levels (%) as compared to the CG group;
the olive oil group (MCao) exhibited decreased enzyme levels
wellbelowthoseintheCGandMCgroups(and%,resp.)
and a decrease of and %, respectively, when compared to
MCac and MCas data. It should be noted that although both
olive oil and avocado oil groups had decreased CK levels, no
signicant eect was observed when compared with MC and
CG groups.
Serumlevelsofhs-CRPintheMCgroupshowedavery
signicant increase (. times) compared to the CG group.
is is consistent with other studies in humans, since it has
been reported that hs-CRP levels are increased in subjects
with signs of health disorders from metabolic abnormality
[]; this increase may also heighten the risk of cardiovas-
cular disease []. Nevertheless, the olive oil group (MCao)
reversed hs-CRP levels, almost reaching CG group levels (.
versus.U/L)butstillwitha.%signicantdierence.
Meanwhile, avocado oil extracted by centrifugation (MCac)
or solvent (MCas) groups reduced hs-CRP levels even more
than olive oil so as to attain levels statistically similar to
the CG group (. and . versus . mg/dL, resp.). As can
beobserved,botholiveoilandavocadooilextractedby
centrifugation or solvent reversed the metabolic changes
induced by sucrose ingestion signicantly and very signi-
cantly reducing hs-CRP levels by % in the MCao group
and by % in the MCac and MCas groups, respectively, as
compared with the MC group. It has been shown that oils rich
in monounsaturated fatty acids do not increase hs-CRP levels
[];instead,theseareloweredinsubjectswhoconsume
a Mediterranean diet, where the main source of monoun-
saturated fatty acids is olive oil []. Other studies show
that elevated hs-CRP levels are directly related to infectious
processes, inammatory response, steatosis, cardiovascular
disease, prevalence, and risk of arteriosclerotic ventricular
thrombosis [,–]; this is why the use of hs-CRP has
been proposed in prognostic stratication in subjects having
health disorders with metabolic abnormalities [].
e inammatory response and its relationship with
atherosclerosis-cardiovascular risk is well demonstrated;
however, it is still under discussion if the measurement
of increased levels of hs-CRP consistently and signicantly
predict cardiovascular risk from a clinical point of view [].
In the present case, one possible explanation of a decrease
in hs-CRP (an inammation biomarker) in a diet with olive
or avocado oil (obtained by any method) could be related to
cytokine inhibition observed in diets with a high oleic acid
content [], considering that interleukin sets o hepatocyte
hs-CRP synthesis [].
To the best of our knowledge, these markers have not been
evaluated in rat models where metabolic changes induced by
sucroseingestionareassociatedwithliverdamagecausedby
abnormalities in liver function. A concentration of normally
metabolized molecules occurs which can have a detrimental
eect on health, hence the importance of these ndings in the
study of the eect of dietary oils such as from avocados.
In conclusion, the results suggest that avocado oil and its
antioxidant content place it as a potential oil to be used as
one of the preventive factors of metabolic syndrome since
it reduces TG, LDL, and VLDL levels, signicantly so in
the case of LDL, without aecting HDL levels. Furthermore
the results indicate that avocado oil exerts eects similar to
olive oil, and that the type of extraction exerts an eect on
only one of the biochemical indicators analyzed. It has also
been found that avocado oil extracted by centrifugation or
solvent decreases hs-CRP levels, indicating that inamma-
tory processes have been at least partially reversed, probably
because the manifestation time of metabolic change was very
short. Further studies are needed to elucidate the eects on
cardiovascular risk prole and inammatory markers and
establish the optimal time of avocado oil supplementation
in rats with sucrose-induced metabolic changes, as well as
the :N specic action on human phospholipid fraction
biosynthesis in HDL as a surface component.
Conflict of Interests
e authors certify that they do not have any conict of
interests regarding the publication of this paper.
References
[] S. Gorinstein, S. Poovarodom, H. Leontowicz et al., “Antioxi-
dant properties and bioactive constituents of some rare exotic
ai fruits and comparison with conventional fruits. In vitro
and in vivo studies,” Food Research International,vol.,no.,
pp. –, .
[] P. Bj¨
orntorp, “Heart and soul: stress and the metabolic syn-
drome,” Scandinavian Cardiovascular Journal,vol.,no.,pp.
–, .
[] G.L.Vega,“Obesity,themetabolicsyndrome,andcardiovas-
cular disease,” American Heart Journal,vol.,no.,pp.–
, .
[] M. W. Steven and G. J. Bruce, “Unsaturated fatty acids,” in Food
Lipids.Chemistry,NutritionandBiotechnology,C.C.Akohand
D. B. Min, Eds., pp. –, Marcel Dekker, New York, NY,
USA, .
[] L.W.Cho,“Metabolicsyndrome,”Singapore Medical Journal,
vol. , no. , pp. –, .
[] A. Ghosh, “e metabolic syndrome: a denition dilemma,”
Cardiovascular Journal of Africa, vol. , no. , pp. –,
.
[] R.B.H.Willis,J.S.K.Lim,andH.Greeneld,“Compositionof
Australian foods: tropical and subtropical fruit,” Food Technol-
ogy in Australia, vol. , pp. –, .
[] B. Bergh, “Nutritious value of Avocado,” in Proceedings of
the Biennial Conference of the Australian Avocado Growers’
Federation. California Avocado Society Book,vol.,pp.–,
Department of Botany and Plant Science, University California,
Riverside, Calif, USA, .
Disease Markers
[] I. Lerman-Garber, S. Ichazo-Cerro, J. Zamora-Gonz´
alez et
al., “Eect of a high-monounsaturated fat diet enriched with
Avocado in NIDDM patients,” Diabetes Care,vol.,no.,pp.
–, .
[]D.Kritchevsky,S.A.Tepper,S.Wrightetal.,“Cholesterol
vehicle in experimental atherosclerosis : Avocado oil,” Journal
of the American College of Nutrition,vol.,no.,pp.–,
.
[] H. Kawagishi, Y. Fukumoto, M. Hatakeyama et al., “Liver injury
suppressing compounds from Avocado (Persea americana),”
Journal of Agricultural and Food Chemistry,vol.,no.,pp.
–, .
[]I.E.Danhof,“Potentialreversalofchronologicalandphoto-
aging of the skin by topical application of natural substances,”
Phytotherapy Research, vol. , pp. S–S, .
[] K. C. Duester, “Avocados,” Nutrition Today,vol.,pp.–,
.
[] Y.F.Lozano,C.D.Mayer,C.Bannonetal.,“Unsaponiable
matter, total sterol and tocopherol contents of Avocado oil
varieties,” JournaloftheAmericanOilChemists’Society,vol.,
no. , pp. –, .
[] J.H.Cohen,A.R.Kristal,andJ.L.Stanford,“Fruitandvegetable
intakes and prostate cancer risk,” Journal of the National Cancer
Institute,vol.,no.,pp.–,.
[] P. G. Reeves, F. H. Nielsen, and G. C. Fahey Jr., “AIN- puried
diets for laboratory rodents: nal report of the American Insti-
tute of Nutrition ad ho c writing committee on the refor mulation
of the AIN-A rodent diet,” Journal of Nutrition,vol.,no.
, pp. –, .
[] R. M. Oliart Ros, M. E. Torres-M´
arquez, A. Badillo et al.,
“Dietary fatty acids eects on sucrose-induced cardiovascular
syndrome in rats,” Journal of Nutritional Biochemistry,vol.,
no. , pp. –, .
[]M.E.Hadi,R.Valdez,andG.Ba
˜
nos, “Possible relationship
between altered fatty acid composition of serum, platelets,
and aorta and hypertension induced by sugar feeding in rats,”
Clinical and Experimental Hypertension,vol.,no.,pp.–
, .
[] G. M. Reaven and H. Chang, “Relationship between blood
pressure, plasma insulin and triglyceride concentration, and
insulin action in spontaneous hypertensive and Wistar-Kyoto
rats,” American Journal of Hypertension,vol.,no.I,pp.–
, .
[] R. M. N. Bezerra, M. Ueno, M. S. Silva et al., “A high fructose
diet aects the early steps of insulin action in muscle and liver
of rats,” Journal of Nutrition,vol.,no.,pp.–,.
[] A. W. orburn, L. H. Storlien, A. B. Jenkins et al., “Fructose-
inducedinvivoinsulinresistanceandelevatedplasmatriglyc-
eride levels in rats,” American Journal of Clinical Nutrition,vol.
, no. , pp. –, .
[] P.M.Piatti,L.D.Monti,L.Barualdietal.,“Eectsofanacute
increase in plasma triglyceride levels on glucose metabolism in
man,” Metabolism,vol.,no.,pp.–,.
[] M. El Hadi, A. Cu´
ellar, J. Ram´
ırez et al., “Eect of sucrose
addition to drinking water, that induces hypertension in the
rats, on liver microsomal ΔandΔ-desaturase activities,”
Journal of Nutritional Biochemistry,vol.,no.,pp.–,
.
[] E. J. Parks and M. K. Hellerstein, “Carbohydrate-induced
hypertriacylglycerolemia: historical perspective and review of
biological mechanisms,” American Journal of Clinical Nutrition,
vol.,no.,pp.–,.
[] J. Carranza, M. Alvizouri, M. R. ´
Alvaro et al., “Efectos del
aguacate sobre los niveles de l´
ıpidos s´
ericos en pacientes
con dislipidemias fenotipo II y IV,” Archivos del Instituto de
Cardiolog´
ıa de M´
exico,vol.,pp.–,.
[] R. L´
opez Ledesma, A. C. Frati Munari, B. C. Hern´
andez
Dom´
ınguez et al., “Monounsaturated fatty acid (Avocado)
rich diet for mild hypercholesterolemia,” Archives of Medical
Research,vol.,no.,pp.–,.
[] E. P´
oveda, P. Ayala, R. Milena et al., “Eects of vegetal oils
supplementation on the lipid prole on Wistar rats,” Biomedica,
vol.,no.,pp.–,.
[] D. Bester, A. J. Esterhuyse, E. J. Truter et al., “Cardiovascular
eects of edible oils: a comparison between four popular edible
oils,” Nutrition Research Reviews,vol.,no.,pp.–,
.
[] S. Heyden, “Polyunsaturated and monounsaturated fatty acid
the diet to prevent coronary heart disease via cholesterol
reduction,” Annals of Nutrition and Metabolism,vol.,no.,
pp.–,.
[] O. P´
erez-M´
endez and L. Gracia-Hern´
andez, “El tama˜
no y la
composici´
on de las lipoprote´
ınas de alta densidad (HDL) se
modica en la rata por una dieta suplementada con aguacate
“Hass”(Persea americana Miller),” Archivos de Cardiolog´
ıa de
M´
exico,vol.,no.,pp.–,.
[] L. B. Dixon and N. D. Ernst, “Choose a diet that is low in
saturatedfatandcholesterolandmoderateintotalfat:subtle
changes to a familiar message,” Journal of Nutrition,vol.,no.
, pp. S–S, .
[]S.Parthasarathy,J.C.Khoo,E.Milleretal.,“Lowdensity
lipoprotein rich in oleic acid is protected agaiinst oxidative
modication: implications for dietary prevention of atheroscle-
rosis,” Proceedings of the National Academy of Sciences of the
United States of America, vol. , no. , pp. –, .
[] M. Abbey, G. B. Belling, M. Noakes et al., “Oxidation of low-
density lipoproteins: intraindividual variability and the eect of
dietary linoleate supplementation,” American Journal of Clinical
Nutrition,vol.,no.,pp.–,.
[]P.Reaven,S.Parthasarathy,B.J.Grasseetal.,“Eectsof
oleate-rich and linoleate-rich diets on the susceptibility of
low density lipoprotein to oxidative modication in mildly
hypercholesterolemic subjects,” Journal of Clinical Investigation,
vol.,no.,pp.–,.
[]P.Mata,O.Varela,R.Alonsoetal.,“Monounsaturatedand
polyunsaturated n- fatty acid-enriched diets modify LDL oxi-
dation and decrease human coronary smooth muscle cell DNA
synthesis,” Arteriosclerosis, rombosis, and Vascular Biology,
vol.,no.,pp.–,.
[] C. Carrillo, M. Ma. del Cavia, and S. Alonso-Torre, “Role of
oleic acid in immune system,mechanism of action, a review,”
Nutrici ´
on Hospitalaria,vol.,no.,pp.–,.
[] M. A. Carluccio, M. Massaro, C. Bonfrate et al., “Oleic acid
inhibits endothelial activation: a direct vascular antiatherogenic
mechanism of a nutritional component in the Mediterranean
diet,” Arteriosclerosis, rombosis, and Vascular Biology,vol.,
no. , pp. –, .
[] A. P. Simopoulos, “e Mediterranean diets: what is so special
about the diet of Greece? e scientic evidence,” Journal of
Nutrition,vol.,no.,pp.S–S,.
[] F. Benkhalti, J. Prost, E. Paz et al., “Eects of feeding virgin olive
oil or their polyphenols on lipid of rat liver,” Nutrition Research,
vol.,no.,pp.–,.
Disease Markers
[] H. E. Anderson, S. V´
azquez Cabrera, R. Lozano et al., “Efecto
del consumo de aguacate (Persea americana Mill) sobre el perl
lip´
ıdico en adultos con dislipidemia,” Anales Venezolanos de
Nutrici ´
on,vol.,no.,pp.–,.
[] P. P´
erez-Mart´
ınez, J. L´
opez-Miranda,J.Delgado-Listaetal.,
“Aceite de oliva y prevenci´
on cardiovascular: m´
as que una
grasa,” Cl´
ınica e Investigaci´
on en Arteriosclerosis,vol.,no.,
pp.–,.
[] M.K.Rutter,J.B.Meigs,L.M.Sullivanetal.,“C-reactivepro-
tein, the metabolic syndrome, and prediction of cardiovascular
events in the Framingham ospring study,” Circulation,vol.,
no. , pp. –, .
[] H. Tomiyama, Y. Koji, M. Yambe et al., “Brachial-ankle pulse
wave velocity is a simple and independent predictor of prog-
nosis in patients with acute coronary syndrome,” Circulation
Journal,vol.,no.,pp.–,.
[] S. Desroches, W. R. Archer, M.-E. Paradis et al., “Baseline
plasma C-reactive protein concentrations inuence lipid and
lipoprotein responses to low-fat and high monounsaturated
fatty acid diets in healthy men,” Journal of Nutrition,vol.,
no. , pp. –, .
[] K. Esposito, R. Marfella, M. Ciotola et al., “Eect of a
Mediterranean-style diet on endothelial dysfunction and mark-
ers of vascular inammation in the metabolic syndrome: a
randomized trial,” JournaloftheAmericanMedicalAssociation,
vol. , no. , pp. –, .
[] M. Fr¨
ohlich, A. Imhof, G. Berg et al., “Association between
C-reactive protein and features of the metabolic syndrome,”
Diabetes Care, vol. , no. , pp. –, .
[] D. A. Morrow and P. M. Ridker, “C-reactive protein, inamma-
tion, and coronary risk,” Medical Clinics of North America,vol.
,no.,pp.–,.
[] M. di Napoli, M. Schwaninger, R. Cappelli et al., “Evaluation
of C-reactive protein measurement for assessing the risk and
prognosis in ischemic stroke: a statement for health care
professionals from the CRP pooling project members,” Stroke,
vol. , no. , pp. –, .
[] N. Lamblin, F. Mouquet, B. Hennache et al., “High-sensitivity
C-reactive protein: potential adjunct for risk stratication in
patients with stable congestive heart failure,” European Heart
Journal,vol.,no.,pp.–,.
[] O.Yousuf,B.D.Mohanty,S.T.Martinetal.,“High-sensitivity
C-reactive protein and cardiovascular disease,” Journal of the
American College of Cardiology,vol.,no.,pp.–,.
[] R. Verlengia, R. Gorj˜
ao, C. C. Kanunfre et al., “Eect of
arachidonic acid on proliferation, cytokines production and
pleiotropic genes expression in Jurkat cells—a comparison with
oleic acid,” Life Sciences, vol. , no. , pp. –, .
[] P. Libby, “Inammation in atherosclerosis,” Nature,vol.,no.
, pp. –, .
Available via license: CC BY
Content may be subject to copyright.