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Purpose: Virgin coconut oil (VCO) is a medium-chain fatty acid source with popularly attributed benefits on obesity management. However, its role on obesity requires elucidation due to its saturated nature. In the study herein, we investigated acute effects of VCO consumption on energy metabolism, cardiometabolic risk markers, and appetitive responses in women with excess body fat. Methods: Fifteen adult women with excess body fat (37.43 ± 0.83%) participated in this randomized, crossover, controlled study. Two isocaloric mixed breakfasts containing 25 mL of VCO or control (extra-virgin olive oil-C) were evaluated. Resting energy expenditure (REE), fat oxidation rate (FOR), diet induced thermogenesis (DIT) and appetitive subjective responses were assessed at fasting and postprandial periods (up to 240 min). Cardiometabolic risk markers were assessed at fasting and up to 180 min postprandially. Results: VCO did not affect REE, FOR, and DIT compared to C. In addition, VCO did not cause deleterious change in triglycerides, total cholesterol, HDL-c, LDL-c, triglycerides/HDL-c ratio, uric acid, glucose and Homeostasis Model Assessment of Insulin Resistance Index (HOMA-IR) (P time×treatment > 0.05). However, VCO suppressed less hunger (P time×treatment = 0.003), total satiety (P iAUC = 0.021) and total fullness (P iAUC = 0.035) responses than C. Conclusions: VCO consumption did not acutely change energy metabolism and cardiometabolic risk markers when added to a mixed breakfast but promoted less appetitive responses.
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Eur J Nutr
DOI 10.1007/s00394-017-1448-5
ORIGINAL CONTRIBUTION
Effects of coconut oil consumption on energy metabolism,
cardiometabolic risk markers, and appetitive responses in women
with excess body fat
Flávia Xavier Valente1 · Flávia Galvão Cândido1 · Lílian Lelis Lopes1 ·
Desirrê Morais Dias1 · Samantha Dalbosco Lins Carvalho1 ·
Patrícia Feliciano Pereira1 · Josefina Bressan1
Received: 23 August 2016 / Accepted: 4 April 2017
© Springer-Verlag Berlin Heidelberg 2017
(Ptime×treatment > 0.05). However, VCO suppressed less hun-
ger (Ptime×treatment = 0.003), total satiety (PiAUC = 0.021)
and total fullness (PiAUC = 0.035) responses than C.
Conclusions VCO consumption did not acutely change
energy metabolism and cardiometabolic risk markers when
added to a mixed breakfast but promoted less appetitive
responses.
Keywords Coconut oil · Energy metabolism · Fat
oxidation · Cardiometabolic risk markers · Appetite
Introduction
Obesity and overweight remain to be a serious public health
problem despite of international efforts to combat them.
Excess body fat is related to non-communicable diseases
(NCDs) such as cardiovascular diseases, hypertension, dia-
betes, and some types of cancer [1]. Data from the latest
World Health Organization report [2] showed that NCDs
have been responsible for around 38 million deaths per
year since 2012, accounting for 68% of all deaths world-
wide. Cardiovascular diseases were the leader in mortality,
which claimed 17.5 million lives in 2012 (46% of all NCDs
deaths), 6 million of which were premature.
Virgin coconut oil (Cocos nucifera L.) (VCO) is a
high quality source of medium-chain fatty acids (MCFA)
with commercial weight loss claims. It has been attrib-
uted to coconut oil thermogenic effects, increased fullness
responses and HDL-c improvement [3, 4]. These are based
on the fact that MCFA could be absorbed and metabolized
faster than others fatty acids [5]. The theory is that faster
metabolization could boost energy and fat metabolism
without promoting fat storage and dyslipidemia and could
enhance satiety [6, 7] thus favoring weight loss. These
Abstract
Purpose Virgin coconut oil (VCO) is a medium-chain fatty
acid source with popularly attributed benefits on obesity
management. However, its role on obesity requires eluci-
dation due to its saturated nature. In the study herein, we
investigated acute effects of VCO consumption on energy
metabolism, cardiometabolic risk markers, and appetitive
responses in women with excess body fat.
Methods Fifteen adult women with excess body fat
(37.43 ± 0.83%) participated in this randomized, crosso-
ver, controlled study. Two isocaloric mixed breakfasts con-
taining 25 mL of VCO or control (extra-virgin olive oil-C)
were evaluated. Resting energy expenditure (REE), fat oxi-
dation rate (FOR), diet induced thermogenesis (DIT) and
appetitive subjective responses were assessed at fasting
and postprandial periods (up to 240 min). Cardiometabolic
risk markers were assessed at fasting and up to 180 min
postprandially.
Results VCO did not affect REE, FOR, and DIT compared
to C. In addition, VCO did not cause deleterious change
in triglycerides, total cholesterol, HDL-c, LDL-c, triglyc-
erides/HDL-c ratio, uric acid, glucose and Homeostasis
Model Assessment of Insulin Resistance Index (HOMA-IR)
Electronic supplementary material The online version of this
article (doi:10.1007/s00394-017-1448-5) contains supplementary
material, which is available to authorized users.
Flávia Xavier Valente and Flávia Galvão Cândido contributed
equally to the manuscript.
* Josefina Bressan
jbressan@ufv.br
1 Departamento de Nutrição e Saúde, Universidade Federal de
Viçosa, Avenida PH Rolfs, s/n., Viçosa, Minas Gerais CEP:
36570-900, Brazil
Eur J Nutr
1 3
claims attract consumers’ attention [8] but it lacks scientific
confirmation.
While some studies reported beneficial effects of coco-
nut oil or isolated MCFA on energy metabolism [9], fat
oxidation [10, 11], food intake [12, 13], and no detrimental
effect on serum cardiometabolic risk markers [1417], oth-
ers demonstrated negative results on lipid profile [18], and
conflicting results on metabolic rates [11, 19], and satiety
[20, 21]. Contradictory results could be partly explained by
the distinct fatty acid composition of VCO compared to the
synthetic source of MCFA adopted in the majority of stud-
ies [9, 1113, 16, 18, 19], enforcing the need for studies
conducted with VCO. Furthermore, randomized controlled
clinical trials about VCO are scarce, present methodologi-
cal limitations such as unusual doses of oil consumption,
and/or exhibit inconclusive results [22].
Because women are the main coconut oil consumers due
to its weight loss claims and previous studies have lead us
to question the applicability of MCFA-rich oil claims in
women [23], the aim of this study was to evaluate acute
effects of reasonable amounts of VCO intake on energy
metabolism, serum cardiometabolic risk markers, and sub-
jective appetitive responses in women with excess body fat.
Methods
Study population
Seventeen women aged 19–42 years with BMI between
25 and 31 kg/m2 and total body fat >32% were recruited
through local advertisement (Supplementary Figure 1).
Exclusion criteria were: known chronic illnesses except
obesity, fasting glucose >5.5 mmol/L, hypertension
(>140/90 mmHg), smoking, alcohol consumption (>2
doses/d), pregnancy or lactation, recent changes (previ-
ous three months) in diet or physical activities habits,
elite athletes (>10 h/week), use of dietary supplements or
drugs except oral contraceptive, food allergies or intoler-
ances, and aversion to the tested ingredients. Based on
published values of fasting fat oxidation and estimated
change of 3.6 g during the postprandial state [24], a sample
size of 12 subjects was estimated for this crossover study
design using the formula by Mera et al. [25]. Account-
ing for dropouts (30%), seventeen subjects have been
enrolled. Participants gave written consent after receiv-
ing verbal and written information. The study was per-
formed at Laboratory of Energy Metabolism and Body
Composition of Nutrition and Health Department, Univer-
sidade Federal de Viçosa, Brazil. The study protocol was
approved by the Ethics Committee of Universidade Federal
de Viçosa (protocol number: 541.836/2014), conducted in
accordance with Helsinki declaration and its later amend-
ments and registered at http://www.ensaiosclinicos.gov.br/
(RBR-8NGPQ9).
Study design
This was a randomized single-blinded crossover design
study in which two different isocaloric breakfasts were
tested in non-consecutive days. Subjects were randomly
assigned by simple draw to either control (extra-virgin
olive oil—EVOO) or VCO breakfast, with washout period
of one week.
Prior to test days, participants were instructed to main-
tain their usual dietary intake and to abstain from alcohol
and strenuous physical activity. On the night before each
test day, all participants consumed standardized dinner
(2.5 MJ; 62E% carbohydrate; 8.5E% protein; 29.4E% fat)
and water intake was allowed until 4 h before starting the
test. Immediately before dinner consumption, participants
emptied their bladder and thenceforth all urine was col-
lected and carried to laboratory.
In each test day, participants attended the laboratory
from 7 a.m. to 1 p.m. after 11 h overnight fasting with
minimal physical effort possible. The remaining 1 h fasting
was completed at laboratory, totaling 12 h of fasting before
test drink consumption. Anthropometric measurements
were recorded by trained appraiser. Body weight was meas-
ured using digital platform scale with resolution of 0.5 kg
(Toledo®, Model 2096PP/2, São Paulo, Brazil), while
participants were barefoot and wearing lightweight cloth-
ing. Height was measured with wall-mounted stadiometer
(Wiso, Chapecó, SC, Brazil) to the closest value to 0.1 cm.
Total body fat was assessed by bioelectrical impedance
(model Y230, InBody Co. Lta., Gyeonggi, Korea). Then,
subjects remained in lay supine for mandatory 15 min
rest period. After that, fasting resting energy expenditure
(REE) and substrate oxidation rates (SOR) were assessed
by indirect calorimetry (Carefusion Vmax® Series, Cal-
ifórnia, EUA) for 30 min and participants remained awake
and motionless as much as possible. This protocol com-
prises fasting REE not very different from a basal energy
expenditure measurement obtained immediately on awak-
ing, after an overnight stay in the laboratory [26]. Urine
was collected to complete 12 h of urine collection. Fasting
(12 h) antecubital blood sample was drawn and subjects
consumed one of two mixed breakfasts containing 25 mL
of control (EVOO) or test (VCO) oils within 15 min. Meal
palatability questionnaire was completed in this period.
Indirect calorimetry followed intermittent protocol pre-
viously developed [27], in which measurements were made
every half for each hour during 4 h following breakfast.
During protocol intervals, subjects remained awake but
inactive and they could not leave the laboratory. Water at
Eur J Nutr
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room temperature (200 mL) was given in each interval and
urine collections were made during all postprandial period.
Antecubital blood samples were collected at 60, 120, and
180 min and subjective appetitive responses were taken
immediately before/after breakfast consumption and imme-
diately before/after each indirect calorimetry until 240 min.
Test breakfasts
Participants were assigned to consume 30 to 40% of their
daily energy requirements as test breakfasts. It consisted of
standard breakfasts containing white bread with 25 mL of
control (EVOO) or test (VCO) oils and 300 mL of milk-
derived fat-free drink (Table 1). Virgin coconut oil (FidBō,
São Paulo, Brazil) and extra-virgin olive oil (Bunge Ali-
mentos, Santa Catarina, Brazil) were maintained protected
from light and heat until consumption and fat-free drink
was offered at ~10 °C.
Fatty acid compositions of EVOO and VCO were
assessed after esterification [29] by gas chromatography
(GC). Chromatographic analysis was carried out using
Shimadzu GC Solution instrument (Shimadzu Seisakusho
Co., Kyoto, Japan) equipped with flame ionization detector
(FID) and Carbowax capillary column (30 m × 0.25 mm).
Briefly, 1µL of esterified sample was injected in GC with
split ratio of 10. Nitrogen was supplied as carrier gas at
flow rate of 43.2 cm/s. The initial oven temperature was
100 °C, maintained for 5 min, then increased to 220 °C
at 4 °C/minutes and held for 20 min. Flow rate over col-
umn was 1.0 mL/minute. FID and injection port tempera-
ture was 200 and 220 °C, respectively. Data handling was
carried out using the software GC Solution package (Shi-
madzu Seisakusho Co., Kyoto, Japan). Fatty acid methyl
esters (FAME) were identified by direct comparison of
retention time with FAME standard mix (Supelco 37 Com-
ponent FAME Mix; Sigma-Aldrich®, EUA).
Energy metabolism measurement and calculation
Flow meter and flow sensor were calibrated daily by a
3.0-L syringe. Analyzers were calibrated with gases of
known concentration before each testing as recommended
by manufacturer’s instructions. The first gas was 26% O2
with N2 balance, the second gas was 4% CO2 16% O2, with
N2, and the last gas was ambient air.
During measurements, subjects had their head covered
with ventilated canopy to quantify oxygen consumed and
carbon dioxide produced. They stayed in quiet room with
stable temperature (22 °C) and humidity (55%) during
measurements. The first 10 min (adaptation phase), and
individual outlier values of oxygen and carbon dioxide
were excluded from the analyses [25, 30]. Means of oxygen
and carbon dioxide volumes (L/min) from the remaining
data were used in the calculations.
REE and SOR (carbohydrate, protein and fat oxidation)
from fasting and postprandial states were calculated using
oxygen and carbon dioxide volumes and urinary nitrogen
excretion of each period of time, as described previously
[31]. Values of non-protein respiratory quotient (NPRQ)
were also calculated [31]. Diet induced thermogenesis
(DIT) was assessed [27] and expressed as percentage of
breakfasts energy. Total urinary nitrogen excretion was esti-
mated by Kjeldahl technique. Changes between fasting and
posprandial carbohydrate and fat oxidation were calculated
by subtracting the total postprandial values over 4 h from
Table 1 Nutritional composition of control and coconut oil break-
fasts
Nutritional information was obtained from manufacturer’s product
information and Brazilian Food Composition Table [28]. Fatty acid
profile was obtained after esterification [29] by gas chromatography
MCFA medium chain fatty acids, LCFA long-chain fatty acids, SFA
saturated fatty acids, MUFA monounsaturated fatty acids, PUFA poly-
unsaturated fatty acids
Control Coconut oil
White bread (g) 50 50
Olive oil (mL) 25
Coconut oil (mL) 25
Powered skim milk (g) 40 40
Strawberry flavoring powder (g) 1 1
Water (mL) 280 280
Energy content (kJ) 494.0 494.0
Carbohydrate (g) 49.0 49.0
(E%) 39.7 39.7
Protein (g) 18.0 18.0
(E%) 14.6 14.6
Total fat (g) 25.0 25.0
(E%) 45.7 45.7
Fatty acid profile (%)
C8:0 – 5.2
C10:0 – 5.4
C12:0 – 51.6
C14:0 – 19.9
C16:0 10.4 8.8
C18:0 2.7 3.0
C18:1 ω9 79.5 5.1
C18:2 ω6 5.6 0.7
C18:3 ω3 0.5 –
Total MCFA 62.3
Total LCFA 100 37.6
Total SFA 13.1 94.0
Total MUFA 80.1 5.1
Total PUFA 6.5 0.7
Fiber (g) 0.0 0.0
Eur J Nutr
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fasting value multiplied by duration of measurement (4 h)
[24].
Cardiometabolic risk markers
Serum samples were separated from whole blood by centrif-
ugation (3500 rpm, 4 °C, 15 min) and immediately frozen at
80 °C until analyses. Triglycerides (TG), total cholesterol,
high-density lipoprotein cholesterol (HDL-c), low-density
lipoprotein cholesterol (LDL-c), glucose, and uric acid were
measured by standard colorimetric kits (K082, K117, K083,
K071, K088, and K139; Bioclin®, Minas Gerais, Brazil) by
automatic biochemical analyzer BS-200 (Mindray Medical
International Ldt., Shenzen, China). Insulin was assessed by
chemiluminescence method. Very low-density lipoprotein
(VLDL) was estimated by Friedewald et al. [32] formula.
Insulin resistance was estimated by Homeostasis Model
Assessment Index of Insulin Resistance (HOMA-IR) using
Matthews et al. [33] equation. Atherogenic Index (TG/HDL
ratio) [34] and total area under the curves (tAUC) of each
cardiometabolic risk marker were also calculated [35].
The normal ranges used for fasting parameters were:
TG (<1.7 mmol/L), total cholesterol (<5.17 mmol/L),
HDL-c (>1.3 mmol/L), LDL-c (<2.6 mmol/L), glucose
(<5.55 mmol/L), uric acid (89.22–475.84 µmol/L), insulin
(<174 pmol/L), and HOMA-IR (<2.7) [36, 37].
Appetitive responses
Hunger (“How hungry do you feel?”), fullness (“How full
do you feel?”), satisfaction (“How satisfied do you feel?”),
and desire to eat specific food types (“Would you like to
eat something sweet?”; “Would you like to eat something
salty?”; “Would you like to eat something savoury?”;
“Would you like to eat something fatty?”) were assessed
using 10 unit visual analog scales (VAS) with words
anchored at their ends, expressing the most positive and the
most negative rating [38]. Incremental area under the curve
(iAUC) was determined for fullness and satiety, and incre-
mental area above the curve (iAAC) was determined for
hunger and desire to eat specific food types. Incremental
areas were assessed by trapezoidal method [35]. VAS were
also used to rate palatability by the following questions:
visual appeal, smell, taste, aftertaste, and palatability [38].
Statistical analysis
Statistical analyses were carried out with SPSS 17 for
Windows (SPSS, Inc., Chicago, IL, USA). Data are
expressed as means and standard errors of the mean
(SEM). Individual outlier values of each variable were
excluded before analyses. Data normality and homo-
scedasticity were assessed by Shapiro–Wilk and Levene
tests, respectively. Non-parametric data were log trans-
formed prior to the analysis. Paired t test was used to
assess significant differences between dietary treatments
for areas under (AUC) or above (AAC) the curve and pal-
atability responses. Repeated-measures ANOVA in mixed
model setting, considering time as within-subject factor
and treatment (breakfast) as between-subject factor were
conducted to verify treatment effects on all variables.
Paired t test with Bonferroni’s correction was performed
to assess differences in individual time-points in which
differences were expected to arise. The α level of 5% was
considered statistically significant.
Results
From the seventeen recruited participants two of them
failed to complete the study protocol due to personal rea-
sons. Both breakfasts were well tolerated by the 15 par-
ticipants. There were no differences between breakfasts
related to palatability questions (P > 0.05). For subjects’
characteristics see Table 2.
Metabolic rates
There were no differences in fasting metabolic rates
between the test days. As expected, there was signifi-
cant time effect in REE, NPRQ, and all SOR (carbohy-
drate, protein, and fat oxidation) (Ptime < 0.001). How-
ever, there were no treatment effect or time × treatment
interaction for any metabolic rate analyzed (Table 3).
Similarly, comparisons of fasting and total postprandial
states for all metabolic parameters showed only effect of
time (Ptime 0.001). Absence of significant results was
Table 2 Baseline characteristics of subjects (n = 15)
Data are presented as mean ± SEM. REE are averaged from baseline
values of each participant at control and VCO test days
BMI body mass index, REE resting energy expenditure
Characteristics Subjects
Age (years) 26.8 ± 1.37
BMI (kg/m2) 27.66 ± 0.44
Waist circumference (cm) 89.89 ± 1.59
Hip circumference (cm) 105.66 ± 0.82
Body fat percentage (%) 37.43 ± 0.83
Lean mass (kg) 24.42 ± 0.54
Fat-free mass (kg) 44.1 ± 0.90
REE (kJ/day) 5392.16 ± 92.56
REE/kg (kJ/day) 76.55 ± 1.08
Eur J Nutr
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maintained when DIT and total postprandial carbohy-
drate and fat oxidation were assessed (Table 3).
Cardiometabolic risk markers
All participants had normal uric acid fasting range
(minimal/maximal: 130.86/285.50 µmol/L). For other
cardiometabolic markers, 13 participants showed nor-
mal fasting range for glucose (minimal/maximal,
4.05/6.49 mmol/L), 13 for insulin (25.7/260.44 pmol/L),
8 for HOMA index (0.75/10.82), 10 for triglycer-
ides (0.46/2.09 mmol/L), 13 for total cholesterol
(3.13/5.72 mmol/L), 8 for HDL-c (0.59/1.99 mmol/L),
and 12 for LDL-c (1.06/3.41 mmol/L). Blood assays
indicated typical middle-aged obesity profile with some
individuals exhibiting disruption in cardiometabolic risk
markers.
There was significant time × treatment interac-
tion for uric acid concentrations between breakfasts
(Ptime×treatment = 0.006); however, such interaction did
not persist after post hoc analysis (P > 0.050). Further-
more, there was trend to time × treatment interaction
in HDL-c levels at time 60 min (Ptime×treatment = 0.055).
There were no significant changes in total postprandial
responses between treatments (Table 4).
Appetitive responses
Analyses of subjective hunger responses showed signifi-
cant time × treatment interaction (Ptime×treatment = 0.003)
with VCO breakfast presenting lesser hunger suppres-
sion at 240 min when compared to control breakfast
(P = 0.019). Further, VCO had significantly lesser total
satiety (PiAUC = 0.021) and total fullness (PiAUC = 0.035)
responses when compared to control (Fig. 1). Additional
questions regarding desire to eat specific food types showed
no significant differences between dietary treatments (Sup-
plementary Fig. 2).
Discussion
During decades, coconut oil consumption was discour-
aged due to its high saturated fat content and consequent
potential to raise blood cholesterol and promote dyslipi-
demia [39]. Analyses of VCO fatty acid composition used
Table 3 Fasting and postprandial energy expenditure and substrate oxidation rates of subjects consuming control or coconut oil (n = 15)
Data were expressed as mean ± SEM. Bold letters indicated significant differences (RM-ANOVA in mixed model setting with time as within-
subject factor and meal as between-subject factor, P < 0.05)
REE resting energy expenditure, NPRQ non-protein respiratory quotient
* Data was analyzed by paired t test
a Calculated as postprandial values over 4 h (fasting value per h × 4)
Meal induced change Control Coconut oil P
Fasting state Postprandial state Fasting state Postprandial state
REE (kJ/day) 5276.08 ± 86.41 5971.99 ± 147.78 5422.52 ± 68,65 5989.97 ± 110.8 Time effect <0.001
Meal effect 0.762
Time × meal 0.227
NPRQ 0.83 ± 0.01 0.86 ± 0.02 0.83 ± 0.01 0.86 ± 0.01 Time effect 0.001
Meal effect 0.816
Time × meal 0.751
Carbohydrate oxidation (g/h) 4.88 ± 0.36 8.06 ± 0.59 4.92 ± 0.34 8.20 ± 0.39 Time effect <0.001
Meal effect 0.555
Time × meal 0.555
Fat oxidation (g/h) 2.59 ± 0.12 2.88 ± 0.19 2.72 ± 0.16 2.70 ± 0.16 Time effect 0.001
Meal effect 0.113
Time × meal 0.117
Protein oxidation (g/h) 2.11 ± 0.18 2.50 ± 0.18 2.14 ± 0.20 2.39 ± 0.20 Time effect <0.001
Meal effect 0.898
Time × meal 0.714
Diet induced thermogenesis (% energy
intake)
4.29 ± 0.51 3.88 ± 0.45 0.483*
Change in carbohydrate oxidation (g/4 h)a 12.24 ± 1.66 12.79 ± 1.46 0.801*
Change in fat oxidation (g/4 h)a11.34 ± 0.52 10.36 ± 0.34 0.240*
Eur J Nutr
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Table 4 Postprandial changes in cardiometabolic risk markers of subjects consuming control or coconut oil (n = 15)
Meal
induced
changes
Control Coconut oil P
Postprandial time (min) AUC* Postprandial time (min) AUC* RM-ANOVA
0 60 120 180 0 60 120 180
Glucose
(mmol/L)
4.51 ± 0.15 4.79 ± 0.20 4.53 ± 0.19 4.49 ± 0.09 812.04 ± 29.11 4.42 ± 0.07 4.94 ± 0.25 4.36 ± 0.16 4.43 ± 0.11 808.06 ± 32.91 Time effect 0.010
Meal effect 0.056
Time × meal 0.335
Insulin
(pmol/L)
84.18 ± 15.10 438.55 ± 53.70 254.83 ± 44.55 169.89 ± 51.96 47726.00 ± 6496.30 62.51 ± 7.26 363.50 ± 38.05 247.09 ± 35.75 175.01 ± 47.42 41958.00 ± 4698.60 Time effect <0.001
Meal effect 0.024
Time × meal 0.640
HOMA-IR 2.63 ± 0.65 13.26 ± 1.82 8.02 ± 1.67 5.18 ± 1.76 1453.79 ± 222.46 1.80 ± 0.23 12.16 ± 1.70 7.17 ± 1.23 5.31 ± 1.62 1326.60 ± 180.61 Time effect <0.001
Meal effect 0.047
Time × meal 0.584
Uric acid
(mmol/L)
0.22 ± 0.01 0.23 ± 0.01 0.22 ± 0.01 0.20 ± 0.01 37.26 ± 2.01 0.22 ± 0.01 0.23 ± 0.01 0.23 ± 0.01 0.21 ± 0.01 39.01 ± 1.88 Time effect <0.001
Meal effect 0.005
Time × meal 0.006
Triglyc-
erides
(mmol/L)
1.33 ± 0.13 1.43 ± 0.14 1.60 ± 0.17 1.46 ± 0.18 257.97 ± 25.19 1.12 ± 0.11 1.34 ± 0.15 1.60 ± 0.19 1.63 ± 0.21 249.33 ± 30.70 Time effect 0.002
Meal effect 0.079
Time × meal 0.083
Total cho-
lesterol
(mmol/L)
4.28 ± 0.16 4.52 ± 0.15 4.38 ± 0.17 4.31 ± 0.18 40.77 ± 5.85 4.00 ± 0.17 4.15 ± 0.14 4.17 ± 0.15 4.20 ± 0.15 31.03 ± 4.42 Time effect <0.001
Meal effect 0.851
Time × meal 0.954
HDL-c
(mmol/L)
1.26 ± 0.10 1.34 ± 0.09 1.27 ± 0.08 1.26 ± 0.06 232.24 ± 13.67 1.26 ± 0.06 1.29 ± 0.07 1.27 ± 0.07 1.26 ± 0.06 223.12 ± 11.61 Time effect 0.015
Meal effect 0.295
Time × meal 0.055
LDL-c
(mmol/L)
2.41 ± 0.13 2.53 ± 0.13 2.38 ± 0.15 2.23 ± 0.18 421.45 ± 23.16 2.23 ± 0.15 2.24 ± 0.15 2.16 ± 0.16 2.20 ± 0.16 391.23 ± 29.97 Time effect 0.306
Meal effect 0.266
Time × meal 0.247
Triglyc-
erides/
HDL-c
1.62 ± 0.16 1.59 ± 0.15 1.62 ± 0.15 1.52 ± 0.08 277.67 ± 22.56 1.43 ± 0.08 1.46 ± 0.09 1.49 ± 0.09 1.51 ± 0.09 260.47 ± 17.80 Time effect 0.210
Meal effect 0.114
Time × meal 0.127
Data were expressed as mean ± SEM. Bold letters indicated significant differences (RM-ANOVA in mixed model setting with time as within-subject factor and meal as between-subject factor,
P < 0.05)
* There were no significant changes (paired t test, P > 0.05)
Eur J Nutr
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in our study support this affirmation since it provided
94% of saturated fat. Nevertheless, we expected that high
proportion of easily oxidized medium-chain fatty acid
(~62% of total saturated fat, 51.6% from lauric acid) could
acutely increase postprandial fat oxidation, resulting in
increased thermogenesis, less detrimental changes in blood
*
-70
-60
-50
-40
-30
-20
-10
0
10
20
015306090 120 150 180 210 240
Changes from baseline VAS (mm)
Time (min.)
How hungry do you feel?
0
10
20
30
40
50
Control Coconut oil
iAAC (mm.min)
0
10
20
30
40
50
60
Control Coconut oil
iAUC (mm.min)
0
10
20
30
40
50
60
70
80
90
100
015306090 120 150 180 210 240
Changes from baseline VAS (mm)
Time (min.)
How satisfied do you feel?
0
10
20
30
40
50
60
70
80
90
015306090 120 150 180 210 240
Changes from baseline VAS (mm
)
Time (min.)
How full do you feel?
0
10
20
30
40
50
60
70
Control Coconut oil
iAUC (mm.min
)
a
b
c
Ptime x treatment = 0.030
P
time xtreatment
= 0.815
*
Ptime x treatment = 0.121
*
Fig. 1 Mean ± SEM changes from baseline of self-reported hun-
ger (a), fullness (b), and satiety (c) responses obtained from visual
analog scales (VAS) in response to extra-virgin olive oil (control)
or virgin coconut oil (test) intake (n = 15). iAUC incremental area
under the curve, iAAC incremental area above the curve. For the sake
of clarity, error bars are only given for the maximum and minimum
values at each time point. Ptime×treatment values were obtained from
RM-ANOVA in mixed model setting with time as within-subject fac-
tor and meal as between-subject factor. *Significantly different from
each other (Paired t test, P < 0.05)
Eur J Nutr
1 3
cardiometabolic risk markers and increased satiety. These
effects could contribute to reduce cardiometabolic risks and
promote long-term weight loss. In fact, it has long been
accepted that MCFA are absorbed and metabolized as rap-
idly as glucose [5, 40] usually accessed for 120 min post-
prandially [41]. For this reason, 240 min would be enough
to evaluate MCFA metabolism.
The hypothesis that an increase in fat oxidation and ther-
mogenesis would occur after VCO consumption was based
on studies showing that acute and long-term consumption
of MCFA, but not whole VCO, resulted in increased fat
oxidation [11, 23, 42, 43] and energy expenditure [23, 43,
44]. However, few prior studies compared acute effects of
VCO on thermogenesis and substrate oxidation rates.
Differences in fatty acid structures, such as chain length,
number and position of unsaturation, and stereoisomeric
configuration affect fatty acid oxidation rate. Hierarchy
seems to exist between saturated and unsaturated fatty
acids when consumed individually. Saturated fatty acids
oxidation rates decrease with increasing chain length [45,
46] while for unsaturated ones, oxidation decreases with an
increase in the number of double bonds [46]. Comparing
unsaturated to saturated fatty acids, the former seems to be
oxidized more rapidly [47] apart from MCFA, which are
oxidized faster than others [48].
In our study, there was no difference between VCO
and EVOO fat oxidation rates when incorporated in usual
mixed breakfasts. Lauric acid (C12:0) is the predominant
MCFA in VCO and it is considered by some authors as a
fatty acid with intermediary properties between MCFA
and LCFA [49]. We believe that high content of lauric
acid in this oil could give it metabolic characteristics more
similar to long-chain fatty acid than MCFA present in syn-
thetic oils (rich in C8:0 and C10:0) adopted in the major-
ity of studies [1113, 1719, 21, 43, 50]. On the other
hand, it was observed increase in carbohydrate oxidation
and decrease in fat oxidation in the first hours after both
breakfasts consumption. However, after 80 min of break-
fast consumption, carbohydrate oxidation started to reduce,
and increase in fat oxidation after VCO breakfast seemed
to occur (Supplementary Fig. 3). Inclusion of carbohydrate
source into breakfasts containing tested oils could change
substrate oxidation profile, once carbohydrates are prefer-
ably oxidized in order to maintain carbohydrate balance. As
consequence, fat oxidation is impaired [51]. Thus, despite
the fact that both groups received equal amounts of carbo-
hydrates, we believe that carbohydrate inclusion could have
delayed fat oxidation response, masking treatment effects
on fat metabolism. We are now testing the role of VCO
added to low carbohydrate meal in energy metabolism.
Our study demonstrated no acutely negative effects of
MCFA-source VCO in triglycerides, total cholesterol, LDL-
c, and triglycerides/HDLc ratio when compared to EVOO
rich in cholesterol-neutral oleic acid. There were great dif-
ferences in the methodology and results from published
randomized clinical trials assessing coconut oil effects, and
not synthetic MCFA, in lipid-related cardiometabolic risk
factors. The majority of these published studies presented
the results of chronic coconut oil consumption and there
were divergent results even when coconut oil doses and
control treatment were similar in different studies [14, 17].
In turn, there was only one published study comparing the
effects of coconut oil consumption to cholesterol-neutral
MUFA [52], but the lack of methodological criteria prevent
us to discuss its results. Some studies published with syn-
thetic MCFA used control fats with cholesterol increasing
[53] or cholesterol decreasing [54], making their results
difficult to interpret. MCFA cholesterol-increasing effects
were observed only when high-doses of MCFA were con-
sumed (e.g., 70 g/d [18] or 43E% [55]). Thus, MCFA
cholesterol-increasing effect could be due to its excessive
consumption and does not reflect the impact of reasonable
doses of MCFA. In the study herein, we showed that acute
consumption of 25 mL of VCO, a reasonable amount to be
consumed without producing undesirable collateral effects
of high-fat meals [14], was not able to cause detrimental
changes on lipid profile. Long-term studies are now needed
to confirm our results.
As well as postprandial dyslipidemia, increased level of
glucose at postprandial state (also referred as postprandial
dysmetabolism) is considered an independent predictor of
future cardiovascular events, even in nondiabetic subjects
[56]. Different fats addition to mixed meals could distinctly
affect carbohydrate digestion and insulin secretion, both
impacting postprandial glycaemia [5759]. Long-chain
saturated fat appears to be the worst type of fat to promote
glycemic control [60]. Because MCFA are hydrolyzed and
absorbed faster than other fats, promote more rapidly gas-
tric emptying, and stimulate less secretion of gut hormones
with insulinotropic properties than long-chain fatty acids
[61, 62], their potential to reduce postprandial glycaemia
have long been neglected. However, Clegg et al. [57] dem-
onstrated that while addition of 22.4 g of long-chain sat-
urated fat (butter) had quite similar glycemic response as
oil-free control, addition of the same amount of MCFA sig-
nificantly reduced almost 40% of total glycemic response,
and this reduction was similar to the addition of MUFA
(olive oil). Our results are in line with these findings since
VCO, high in MCFA, presented the same impact as EVOO
on postprandial glycaemia.
MCFA influence on satiety was assessed in few studies
[12, 13, 20, 21, 63, 64] and the majority enrolled normal
weight subjects [12, 13, 20]. Only one was conducted in
normal weight to overweight subjects [21]. Reports from
published studies failed to demonstrate MCFA effect on
appetite suppression [12, 13, 20, 21, 63, 64], despite some
Eur J Nutr
1 3
showed decreased food intake in subsequent meals [12,
13]. In the current study, we investigated VCO effects
on subjective appetitive responses in overweight/obese
women. Our study consistently showed that VCO addi-
tion to mixed breakfast promoted lesser satiating responses
than control breakfast containing similar dose of EVOO
rich in long-chain fatty acids. Results were characterized
by reduced suppression of total hunger, fullness, and sati-
ating responses, and were independent of palatability dif-
ferences. These findings refute our previous hypothesis that
VCO could increase satiety and, for this reason, reduce
food intake contributing for weight loss.
Our study presented several strengths. First we prop-
erly used EVOO as control which is a natural source of the
cholesterol-neutral oleic acid. Furthermore, we assessed
the effects of a dietary source of MCFA, and not synthetic
MCFA source, on energy metabolism, cardiometabolic risk
markers, and satiety. This could improve the clinical impli-
cations of our findings, once VCO is the main commercial
MCFA source which is largely available for population con-
sumption worldwide. Also, the only difference between test
and control breakfasts was the added oil. Finally, our study
differed from most previous studies because it enrolled over-
weight/obese women and used reasonable dose of VCO.
Our study also has limitations. Despite of assessing
metabolic rates for 240 min postprandially was consid-
ered adequate in several published studies, it is possible
that this period of time was not enough to detect differ-
ences in fat oxidation between fat meals in presence of
carbohydrate. Furthermore, it could not be neglected that
240 min may be not enough to detect changes in some
serum lipid fractions in control group.
Conclusion
Inclusion of reasonable amount (25 mL) of virgin coco-
nut oil into mixed breakfast did not affect energy metabo-
lism, fat oxidation rates, and cardiometabolic risk markers
compared to similar control breakfast in generally healthy
excess body fat women. Furthermore, this oil suppressed
less the hunger, satiety, and fullness responses suggesting
that VCO consumption is not effective in improving energy
balance. Thus, we recommend caution in prescribing coco-
nut oil as adjuvant in weight loss programs. Long-term
studies assessing the role of VCO in obesity control are
now necessary to confirm our results.
Acknowledgements We thank Dr. Orgânico, company affiliated
to the FidBō group, for kindly donate virgin coconut oil for this
research. We also thank Bioclin® for providing biochemical assays
kits and Fundação de Amparo à Pesquisa do Estado de Minas Ger-
ais—FAPEMIG, Coordenação de Aperfeiçoamento de Pessoal de
Nível Superior—CAPES, and Conselho Nacional de Desenvolvi-
mento Científico e Tecnológico—CNPq for financial support. These
companies had no role in manuscript design, analysis, or writing.
Compliance with ethical standards
Ethical standards The study protocol was approved by the Eth-
ics Committee of Universidade Federal de Viçosa (protocol num-
ber: 541,836/2014), conducted in accordance with 1964 Declaration
of Helsinki and its later amendments and registered at http://www.
ensaiosclinicos.gov.br/(RBR-8NGPQ9). All participants gave written
consent after receiving verbal and written information.
Conflict of interest The authors declare that they have no conflict of
interest.
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... For example, Zacek et al. have shown that an HF diet supplemented with coconut oil reduced IR in mice [11]. In other studies, coconut oil as a fat source in diet did not promote IR in rodents and humans [38][39][40]. Our data show that specific LA supplementation caused less IR compared to PA supplementation in diet, further suggesting that MCSFAs have a favorable effect in controlling metabolic disorders compared to LCSFAs. ...
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Simple Summary: The aim of this study was to compare the effect of palmitic acid (PA), a long-chain fatty acid, and lauric acid (LA), a medium-chain fatty acid, on obesity-related metabolic disorders. We used a mouse model of diet-induced obesity and fed them a modified high fat diet supplemented with 3% PA or LA for 12 wk. An LA diet led to an increase in visceral fat mass with a reduction in inflammation compared to the PA diet. We also noted that PA significantly increased systemic insulin resistance whereas LA showed only a trend towards an increase compared to lean control mice. The expression of a protein involved in muscle glucose uptake was higher in LA-treated mice compared to the PA-treated group, indicating improved muscle glucose uptake in LA-fed mice. Analysis of liver samples showed that hepatic steatosis was higher in both PA and LA-fed mice compared to lean controls. Markers of liver inflammation were not altered significantly in mice receiving PA or LA. Our data suggest that compared to PA, LA exerts less adverse effects on metabolic disorders and this could be due to the differential effects of these fatty acids in fat and muscle. Abstract: Coconut oil, rich in medium-chain saturated fatty acids (MCSFA), in particular, lauric acid (LA), is known to exert beneficial metabolic effects. Although LA is the most abundant saturated fatty acid in coconut oil, the specific role of LA in altering obesity-related metabolic disorders remains unknown. Here, we examined the effects of supplementing a high fat (HF) diet with purified LA on obesity-associated metabolic derangements in comparison with palmitic acid (PA), a long-chain saturated fatty acid. Male C57BL/6 mice were fed a control chow diet (CD) or an HF diet supplemented with 3% LA (HF + LA) or PA (HF + PA) for 12 wk. Markers of adipose tissue (AT) inflammation, systemic insulin resistance (IR), and hepatic steatosis, were assessed. The body weight and total fat mass were significantly higher in both HF + LA and HF + PA diet-fed groups compared to CD controls. However, the visceral adipose tissue (VAT) mass was significantly higher (p < 0.001) in HF + LA-fed mice compared to both CD as well as HF + PA-fed mice. Interestingly, markers of AT inflammation were promoted to a lesser extent in HF + LA-fed mice compared to HF + PA-fed mice. Thus, immunohistochemical analysis of VAT showed an increase in MCP-1 and IL-6 staining in HF + PA-fed mice but not in HF + LA-fed mice compared to CD controls. Further, the mRNA levels of macrophage and inflammatory markers were significantly higher in HF + PA-fed mice (p < 0.001) whereas these markers were increased to a lesser extent in HF + LA-fed group. Of note, the insulin tolerance test revealed that IR was significantly increased only in HF + PA-fed mice but not in HF + LA-fed group compared to CD controls. While liver triglycerides were increased Biology 2020, 9, 346 2 of 17 significantly in both HF + PA and HF + LA-fed mice, liver weight and plasma markers of liver injury such as alanine aminotransferase and aspartate aminotransferase were increased significantly only in HF + PA-fed mice but not in HF + LA-fed mice. Taken together, our data suggest that although both LA and PA increased AT inflammation, systemic IR, and liver injury, the extent of metabolic derangements caused by LA was less compared to PA in the setting of high fat feeding.
... Hence the study failed to conclude an impact of VCO consumption on weight control. Further, Xavier et al. 77 evaluated the effect of consumption of VCO and extra-virgin olive oil on energy metabolism, fat oxidation rates and cardiometabolic risk markers in 17 women aged between 19 and 42. The authors reported that there was no difference in the above parameters studied between the two groups yet lower hunger suppression, satiety and total fullness were observed for the VCO-ingested group. ...
... A study done by Valente et al in Brazil have found that no such association exists. 32 But dietary consumption of coconut oil reduces the appetite. ...
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Background: Obesity has emerged as one of the major health problems in recent years. This increasing prevalence has implications in health issues in later parts of life. Life style factors and diet practices are the attributed factors to the development of obesity.Methods: This cross sectional study was conducted among 1011 adolescent school children in Kozhikode corporation area, Kerala, South India after getting necessary permissions. A semi structured questionnaire which contained questions related to socio demographic characters, diet, physical activity and other known risk factors of obesity in adolescents was administered.Results: 76.8% of the study subjects were of normal weight, while 15.5% were underweight (thinness- 9% and severe thinness- 6.5%). 1.9% were obese and 5.8% were overweight. The combined prevalence of overweight and obesity was 7.7%. Nuclear family, better family education, better SES, skipping breakfast and consumption of more sweets were associated with obesity.Conclusions: Preventive and promotive measures to reduce the burden of obesity needs to be initiated from early childhood and must be insisted to the family members also. School based lifestyles and behavioural change measures, encouraging school teachers to actively participate in these measures, active involvement of school children in regular sports activities, periodic anthropometric assessment and intervention when needed along with sensitization of parents towards the consequences of obesity are some of the measures to prevent the rising epidemic.
... for iAUC (36 comparisons) (Supplemental Figure 8) (21,(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62)(63)(64)(65), indicative of a significant ppTG-lowering effect, whereas the Hedges' g value reflected 0.16 (95% CI: 0.06, 0.26) with I 2 = 35.8% for AUC (18 comparisons) (Supplemental Figure 9) (54,59,61,(66)(67)(68)(69)(70)(71), indicative of a significant ppTG-raising effect. The overall pooled SMD was −0.23 (95% CI: −0.58, 0.12) with I 2 = 0.0% for C max change values (7 comparisons) (Supplemental Figure 10) (21,58,72). ...
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The use of postprandial triglyceride (ppTG) as a cardiovascular disease risk indicator has gained recent popularity. However, the influence of different foods or food ingredients on the ppTG response has not been comprehensively characterized. A systematic literature review and meta-analysis was conducted to assess the effects of foods or food ingredients on the ppTG response. PubMed, MEDLINE, Cochrane, and CINAHL databases were searched for relevant acute (<24-h) randomized controlled trials published up to September 2018. Based on our selection criteria, 179 relevant trials (366 comparisons) were identified and systematically compiled into distinct food or food ingredient categories. A ppTG-lowering effect was noted for soluble fiber (Hedges' giAUC = -0.72; 95% CI: -1.33, -0.11), sodium bicarbonate mineral water (Hedges' gAUC = -0.42; 95% CI: -0.79, -0.04), diacylglycerol oil (Hedges' giAUC = -0.38; 95% CI: -0.75, -0.00), and whey protein when it was contrasted with other proteins. The fats group showed significant but opposite effects depending on the outcome measure used (Hedges' giAUC = -0.32; 95% CI: -0.61, -0.03; and Hedges' gAUC = 0.16; 95% CI: 0.06, 0.26). Data for other important food groups (nuts, vegetables, and polyphenols) were also assessed but of limited availability. Assessing for oral fat tolerance test (OFTT) recommendation compliance, most trials were ≥4 h long but lacked a sufficiently high fat challenge. iAUC and AUC were more common measures of ppTG. Overall, our analyses indicate that the effects on ppTG by different food groups are diverse, largely influenced by the type of food or food ingredient within the same group. The type of ppTG measurement can also influence the response.
... 11 Penurunan kadar lemak tubuh ini tampaknya disebabkan oleh berkurangnya nafsu makan. 12 Dengan tingginya konsumsi VCO sebagai suplemen diet, terutama diet rendah karbohidrat, maka perlu diteliti apakah pemberian VCO sebanyak 5 ml per kilogram berat badan selama satu bulan dapat bermanfaat dalam memperbaiki parameter antropometrik dan metabolik, terlebih karena VCO adalah suplemen yang cukup aman dan mudah didapatkan di masyarakat. ...
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Latar Belakang: Untuk mengatasi masalah obesitas ada banyak program modifikasi gaya hidup melalui pengaturan pola makan dan peningkatan aktivitas fisik. Di antara program diet dikenal diet rendah lemak serta derivatnya dan diet rendah karbohidrat. Beberapa penelitian menunjukkan bahwa efek positif diet rendah karbohidrat sebagian besar diperantarai oleh keton dalam darah. Selain dapat berfungsi sebagai sumber energi alternatif yang efisien, keton dapat berperan juga sebagai molekul sinyal yang dapat mempengaruhi metabolisme sel dan perilaku. Virgin Coconut Oil (VCO) adalah sumber asam lemak rantai sedang alamiah dengan kuantitas dan kualitas tinggi yang dapat diserap dan dimetabolisme di dalam liver dengan mudah dan cepat menjadi keton Tujuan: Penelitian ini dilakukan untuk mengetahui efek suplementasi virgin coconut oil terhadap kadar glukosa darah, keton darah, asupan makanan, massa lemak viseral dan berat badan pada model obesitas yang diinduksi melalui diet tinggi lemak-sukrosa.Metode: Tiga puluh dua subyek tikus wistar jantan yang sebelumnya sudah dibuat obesitas (indeks Lee >0,300) melalui diet tinggi lemak-sukrosa selama 20 minggu dibagi ke dalam empat kelompok. Kelompok (A) mendapat akuades per oral, kelompok (S) mendapat larutan sukrosa per oral, kelompok (VCO) mendapat VCO per oral, dan kelompok (CO) mendapat minyak jagung per oral selama 4 minggu, diberikan sebelum makan pada siklus malam tikus.Hasil: Hasil penelitian menunjukkan tidak ada perbedaan bermakna pada kadar glukosa darah, massa lemak viseral dan berat badan antar kelompok subyek. Hasil penelitian menunjukkan bahwa pemberian virgin coconut oil dapat meningkatkan kadar keton darah dan menurunkan asupan makanan (p=0,023 dan p=0,000) dibandingkan dengan kelompok perlakuan lain.Simpulan: Hasil penelitian menunjukkan bahwa suplementasi VCO sebelum makan dapat meningkatkan kadar keton darah dan menekan asupan makanan tikus obesitas yang diinduksi diet tinggi lemak-sukros. Namun, penurunan asupan makanan tampaknya tidak dipengaruhi oleh kadar keton dalam darah.
... In studies on the human consumption of virgin coconut oil, Voon et al. [8] found no alteration in the thrombogenicity indices: cellular adhesion molecules, thromboxane B2 (TXB2) and the TXB2/protacyclin ratio in healthy Malaysian adults. Similarly, Valente et al. [9] found no change in energy metabolism and cardiometabolic risk markers in women with excess body fat after the acute consumption of an isocaloric mixed breakfast containing 25 ml of virgin coconut oil compared to a control group, but the breakfast promoted less appetitive response. However, Cardoso et al. [10] found that a virgin coconut oil-rich diet caused increases in HDL cholesterol and a decreased waist circumference and body mass in coronary artery disease patients. ...
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Background: Coconut milk consumption in middle-aged male rats can cause increased blood vessel endothelial nitric oxide synthase (eNOS) and cystathionine-γ-lyase (CSE) protein expression, and decreased fasting blood glucose. Objective: The present study aimed to investigate whether coconut milk oil (CO), the major constituents of the coconut milk, was responsible for those effects. Methods: CO was isolated from dried fresh coconut milk and gavaged (1 and 3 ml/kg) to middle-aged male rats for 6 weeks. Animal body weight and food intake, internal organ weight, blood biochemistry, lipid profile, basal blood pressure and heart rate and vascular functions were investigated. Results: In comparison to a distilled water control group, no differences were observed in any of the parameters studied in the group fed 1 ml/kg of CO except for an increase in retroperitoneal fat accumulation. Feeding 3 ml/kg of CO caused decreased fasting blood glucose, plasma alkaline phosphatase and blood urea nitrogen and liver cell lipid accumulation, but increased retroperitoneal fat tissue. It also caused decreased maximal contractile response of endothelium-intact thoracic aortic rings to phenylephrine although the effect disappeared in the presence of N-nitro-L-arginine (L-NA) or removal of the endothelium. DL-propargylglycine together with L-NA caused a higher contraction to phenylephrine in the CO-treated groups than in the control group. It also caused an increase in vasodilatation to acetylcholine, but not to glyceryl trinitrate, of the phenylephrine pre-contracted aortic rings. CO treatment caused increased vascular wall eNOS and CSE protein expression. Conclusion: CO at a dose of 3 ml/kg causes some decrease in cardiovascular risk factors in middle-aged male rats, although the amount of CO consumption should be limited as it caused an increase in retroperitoneal fat. Keywords: Coconut oil; blood vessel; liver lipid; NO; H2S
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Background: Coconut oil appears to help to the weight loss and improve metabolic parameters associated with obesity. We evaluate the influence of coconut oil on body composition, lipid profile and glycemia in men with obesity. Methods: Controlled, randomized clinical trial was performed with 29 adult men affected by obesity. They were randomized between two groups receiving daily intake of 1 tablespoon (12 mL) of extra virgin coconut oil (CO, n=15) or soybean oil (SO, n=14), and isoenergetic balanced diet. Anthropometric, lipid profile and glycaemia were evaluated at baseline and 45 days after intervention. Mann-Whitney test was performed to compare the groups, and Wilcoxon test to compare before and after intervention. We considered significant p<0.05. Results: There was no difference in anthropometric variables between the groups before and after intervention. Change in HDL-cholesterol increased (3.67±8.08 versus -3.79±10.98, p=0.02) and TC/HDL-cholesterol ratio decreased (-0.63±0.82 versus 0.23±0.80, p=0.03) in CO, compared to SO. Conclusion: Coconut oil inserted into the isoenergetic balanced diet could increase HDL-cholesterol and decrease TC/HDL-cholesterol ratio in men with obesity.
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Scope Eating large amounts of fat is usually associated with fat accumulation. However, different types of diets (not only lipids) elicit different metabolic responses. Methods and results Male and female rats (10wk‐old) were distributed in four groups and fed for one‐month a standard diet (SD), or this diet enriched with either lipid (high‐fat diet, HF) or protein (high‐protein diet, HP), or a cafeteria diet (CAF). Both HF and CAF diets shared the percentage of energy from lipids (40%) but these were different. Protein‐derived energy in the HP diet was also 40%. Feeding SD, HF and HP diets did not result in differences in energy intake, energy expenditure, total body weight or lipid content. However, the CAF fed groups showed increases in these parameters, which were more marked in the male rats. The CAF diet increased the mass of adipose tissue while the HF diet did not. Conclusions Different diets produced substantial changes in the fate of ingested nutrient energy. Dietary lipids were not essential for sustaining increases in body lipid (or adipose tissue) content. Body protein accrual was unrelated to dietary lipids and overall energy intake. Both protein and lipid accrual were more efficient in male than in female rats. This article is protected by copyright. All rights reserved
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Research has indicated that consuming medium-chain triglycerides (MCT) may be more satiating than consuming long-chain triglycerides (LCT) potentially causing a reduction in energy intake. However not all studies have demonstrated this acute reduction in energy intake and it has yet to be systematically reviewed. Our main objective was to examine how ingestion of MCT influences energy intake, subjective appetite ratings and appetite-related hormones compared to LCT. Web of Science, MEDLINE, CINHAL, and Embase were searched for publications comparing the effect of MCT on appetite (commonly hunger, fullness, desire to eat, and prospective food consumption), appetite-related hormones (pancreatic polypeptide (PP), gastric inhibitory polypeptide (GIP), peptide YY (PYY), glucagon-like peptide-1 (GLP-1), neurotensin, leptin, total ghrelin and active ghrelin) and energy intake to LCT. A random-effects meta-analysis was conducted on studies which examined energy intake. Seventeen studies (291 participants) were included in the systematic review, of which 11 were included in the energy intake meta-analysis. Synthesis of combined data showed evidence of a statistically significant moderate decrease in ad libitum energy intake after both acute and chronic ingestion of MCT compared to LCT when assessed under laboratory conditions (mean effect size: −0.444, 95% CI −0.808, −0.080, p < 0.017), despite little evidence of any effect of MCT on subjective appetite ratings or circulating hormones. The current evidence supports the notion that MCT decreases subsequent energy intake, but does not appear to affect appetite. Further research is warranted to elucidate the mechanisms by which MCT reduce energy intake.
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Context: Coconut oil is rich in medium-chain fatty acids and has been claimed to have numerous health benefits. Objective: This review aimed to examine the evidence surrounding coconut oil consumption and its impact on cardiovascular health. Data sources: A systematic literature search of the PubMed, Embase, the Cochrane Library, and CINAHL databases, up to May 2019, was performed. Data extraction: Study characteristics including study design, population, intervention, comparator, outcome, and source of funding were summarized. Data analysis: Meta-analyses included 12 studies to provide estimates of effects. Subgroup analyses were performed to account for any differences in the study-level characteristics. When compared with plant oils and animal oils, coconut oil was found to significantly increase high-density lipoprotein cholesterol (HDL-C) by 0.57 mg/dL (95%CI, 0.40-0.74 mg/dL; I2 = 6.7%) and 0.33 mg/dL (0.01-0.65 mg/dL; I2 = 0%), respectively. Coconut oil significantly raised low-density lipoprotein cholesterol (LDL-C) by 0.26 mg/dL (0.09-0.43 mg/dL; I2 = 59.7%) compared with plant oils and lowered LDL-C (-0.37 mg/dL; -0.69 to -0.05 mg/dL; I2 = 48.1%) compared with animal oils. No significant effects on triglyceride were observed. Better lipid profiles were demonstrated with the virgin form of coconut oil. Conclusion: Compared with animal oils, coconut oil demonstrated a better lipid profile n comparison with plant oils, coconut oil significantly increased HDL-C and LDL-C.
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Coconut oil is being heavily promoted as a healthy oil, with benefits that include support of heart health. To assess the merits of this claim, the literature on the effect of coconut consumption on cardiovascular risk factors and outcomes in humans was reviewed. Twenty-one research papers were identified for inclusion in the review: 8 clinical trials and 13 observational studies. The majority examined the effect of coconut oil or coconut products on serum lipid profiles. Coconut oil generally raised total and low-density lipoprotein cholesterol to a greater extent than cis unsaturated plant oils, but to a lesser extent than butter. The effect of coconut consumption on the ratio of total cholesterol to high-density lipoprotein cholesterol was often not examined. Observational evidence suggests that consumption of coconut flesh or squeezed coconut in the context of traditional dietary patterns does not lead to adverse cardiovascular outcomes. However, due to large differences in dietary and lifestyle patterns, these findings cannot be applied to a typical Western diet. Overall, the weight of the evidence from intervention studies to date suggests that replacing coconut oil with cis unsaturated fats would alter blood lipid profiles in a manner consistent with a reduction in risk factors for cardiovascular disease.
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Background and rationale: Coronary artery disease (CAD) and its pathological atherosclerotic process are closely related to lipids. Lipids levels are in turn influenced by dietary oils and fats. Saturated fatty acids increase the risk for atherosclerosis by increasing the cholesterol level. This study was conducted to investigate the impact of cooking oil media (coconut oil and sunflower oil) on lipid profile, antioxidant mechanism, and endothelial function in patients with established CAD. Design and methods: In a single center randomized study in India, patients with stable CAD on standard medical care were assigned to receive coconut oil (Group I) or sunflower oil (Group II) as cooking media for 2 years. Anthropometric measurements, serum, lipids, Lipoprotein a, apo B/A-1 ratio, antioxidants, flow-mediated vasodilation, and cardiovascular events were assessed at 3 months, 6 months, 1 year, and 2 years. Results: Hundred patients in each arm completed 2 years with 98% follow-up. There was no statistically significant difference in the anthropometric, biochemical, vascular function, and in cardiovascular events after 2 years. Conclusion: Coconut oil even though rich in saturated fatty acids in comparison to sunflower oil when used as cooking oil media over a period of 2 years did not change the lipid-related cardiovascular risk factors and events in those receiving standard medical care.
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Objectives: To review the contribution of the Nurses' Health Studies (NHS and NHS II) in addressing hypotheses regarding risk factors for and consequences of obesity. Methods: Narrative review of the publications of the NHS and NHS II between 1976 and 2016. Results: Long-term NHS research has shown that weight gain and being overweight or obese are important risk factors for type 2 diabetes, cardiovascular diseases, certain types of cancers, and premature death. The cohorts have elucidated the role of dietary and lifestyle factors in obesity, especially sugar-sweetened beverages, poor diet quality, physical inactivity, prolonged screen time, short sleep duration or shift work, and built environment characteristics. Genome-wide association and gene-lifestyle interaction studies have shown that genetic factors predispose individuals to obesity but that such susceptibility can be attenuated by healthy lifestyle choices. This research has contributed to evolving clinical and public health guidelines on the importance of limiting weight gain through healthy dietary and lifestyle behaviors. Conclusions: The NHS cohorts have contributed to our understanding of the risk factors for and consequences of obesity and made a lasting impact on clinical and public health guidelines on obesity prevention. (Am J Public Health. Published online ahead of print July 26, 2016: e1-e7. doi:10.2105/AJPH.2016.303326).
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Effects of different oils on physicochemical properties, consumer liking, emotion, and purchase intent of sponge cakes were evaluated. Three healthy oils (extra virgin coconut oil, EVCO; extra virgin olive oil, EVOO; rice bran oil, RBO) compared with butter (the control), were used at 20% (w/w, wheat flour basis) in sponge cake formulations. Five positive (calm, good, happy, pleased, satisfied) and 3 negative (guilty, unsafe, worried) emotion terms, selected from the EsSense Profile(®) with slight modification using an online (N = 234) check-all-that-apply questionnaire, were used for consumer testing. Consumers (N = 148) evaluated acceptability of 9 sensory attributes on a 9-point hedonic scale, 8 emotion responses on a 5-point rating scale, and purchase intent on a binomial scale. Overall liking, emotion, and purchase intent were evaluated before compared with after health benefit statement of oils had been given to consumers. Overall liking and positive emotion (except calm) scores of sponge cake made with EVCO were higher than those made with EVOO and RBO. Specific volume, expansion ratio, and moisture content of control, EVCO, and EVOO were not significantly different, but higher than RBO sponge cake. JAR results showed that sponge cake made with RBO had the least softness that was reflected by the highest hardness (6.61 to 9.69 compared with. 12.76N). Oil (EVCO/EVOO/RBO) health benefit statement provided to consumer significantly increased overall liking, positive emotion, and purchase intent scores while decreased negative emotion scores. Overall liking and pleased emotion were critical attributes influencing purchase intent (odds ratio = 2.06 to 3.75), whereas calm and happy became not critical after health benefit statement had been given.
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Emphasis on diet to improve the cardiovascular (CV) risk profile has been the focus of many studies. Recently, virgin coconut oil (VCO) has been growing in popularity due to its potential CV benefits. The chemical properties and the manufacturing process of VCO make this oil healthier than its copra-derived counterpart. This review highlights the mechanism through which saturated fatty acids contribute to CV disease (CVD), how oils and fats contribute to the risk of CVD, and the existing views on VCO and how its cardioprotective effects may make this a possible dietary intervention in isolation or in combination with exercise to help reduce the burden of CVDs