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931
Nutr Hosp. 2015;32(2):931-945
ISSN 0212-1611 • CODEN NUHOEQ
S.V.R. 318
Original / Otros
The consumption of acai pulp changes the concentrations of plasminogen
activator inhibitor-1 and epidermal growth factor (EGF) in apparently
healthy women
Izabelle de Sousa Pereira1, Tereza Cristina Moreira Cançado Mascarenhas Pontes1,
Renata Adrielle Lima Vieira1, Gilce Andrezza de Freitas Folly1, Fernanda Cacilda Silva2,
Fernando Luiz Pereira de Oliveira3, Joana Ferreira do Amaral4 ,Renata Nascimento de Freitas5
and Ana Carolina Pinheiro Volp6
1MSc. in Health and Nutrition by Federal University of Ouro Preto, Ouro Preto, Minas Gerais. 2PhD in Biological Science and
Postdoctoral researcher in Cardiovascular Physiology Laboratory at Federal University of Ouro Preto, Ouro Preto, Minas
Gerais. 3PhD in Statistics, Department of Statistics, Federal University of Ouro Preto, Ouro Preto. 4PhD in Biochemistry and
Immunology and Adjunct Professor at the Federal University of Ouro Preto, Ouro Preto, Minas Gerais. 5PhD in Biochemistry
and Immunology and Associated Professor at the Federal University of Ouro Preto, Ouro Preto, Minas Gerais. 6PhD in Science
and Technology of Food and Adjunct Professor at Universidade Federal de Ouro Preto, Ouro Preto, MG (Brazil).
Abstract
Introduction: obesity, characterized by adiposity ex-
cess, is associated with endothelial dysfunction and pos-
sible inflammatory state with release of cytokines that
determine endothelial function and can trigger chronic
diseases. The dietary pattern are associated with the syn-
thesis these cytokines. Fruits as the acai, which is rich in
flavonoids, have a direct and beneficial effect on the con-
trol of this inflammatory process through the exercised
antioxidant capacity.
Objective: to evaluate the effect of acai pulp consump-
tion on the inflammatory markers, anthropometric me-
asurements, body composition, biochemical and dietary
parameters in healthy women.
Methods: forty women, were divided in 25 eutrophic
and 15 with overweight. They intaked 200 g of acai pulp
during 4 weeks. Anthropometric measurements, body
composition, inflammatory markers, biochemical data,
dietary intake and dietary antioxidants capacity were
evaluated before and after the intervention.
Results and discussion: after the intervention, the-
re was significant increase of EGF (p = 0.021) and PAI-
1(p = 0.011) in overweight women. Moreover, there was
increase in body weight (p = 0.031), body mass index
(p = 0.028), percentage of truncal fat (p = 0.003) and tri-
ceps skinfold thickness (p = 0.046) in eutrophic women.
EL CONSUMO DE PULPA ACAI CAMBIA LAS
CONCENTRACIONES DE ACTIVADOR DEL
PLASMINÓGENO INHIBIDOR 1 Y FACTOR
DE CRECIMIENTO EPIDÉRMICO (EGF) EN
MUJERES APARENTEMENTE SANAS
Resumen
Introducción: la obesidad, que se caracteriza por el ex-
ceso de adiposidad, se asocia con disfunción endotelial y
posible estado inflamatorio con liberación de citoquinas
que determinan la función endotelial y pueden desen-
cadenar enfermedades crónicas. El patrón de dieta está
asociado con la síntesis de estas citoquinas. Los frutos de
el acai, que es rico en flavonoides, tienen un efecto directo
y positivo en el control de este proceso inflamatorio a tra-
vés de los ejercicios de la capacidad antioxidante.
Objetivo: evaluar el efecto del consumo de pulpa de
acai en los marcadores inflamatorios, las medidas an-
tropométricas, la composición corporal y los parámetros
bioquímicos y dietéticos en mujeres sanas.
Métodos: cuarenta mujeres fueron divididas en 25
eutróficas y 15 con sobrepeso. Se las adeministró 200 g
de pulpa de acai durante 4 semanas. Antes y después de
la intervención se evaluaron: medidas antropométricas,
composición corporal, marcadores inflamatorios, datos
bioquímicos, ingesta dietética y antioxidantes en la dieta.
Resultados y discusión: después de la intervención,
hubo un aumento significativo de EGF (p = 0,021) y PAI-1
(p = 0,011) en las mujeres con sobrepeso. Por otra parte,
en las mujeres eutróficas hubo aumento del peso corpo-
ral (p = 0,031), el índice de masa corporal (p = 0,028), el
porcentaje de grasa del tronco (p = 0,003) y el espesor del
pliegue cutáneo del tríceps (p = 0,046). Sin embargo, el es-
pesor del pliegue cutáneo (p = 0,018) y la grasa corporal
total (p = 0,016) se redujeron en las mujeres con sobre-
Correspondence: Ana Carolina Pinheiro Volp.
Departamento de Clínica y la Nutrición.
Escuela Social de Nutrición de la
Universidad Federal de Ouro Preto, Brasil.
Campus Universitario, Morro do Cruzeiro, s/nº.
Ouro Preto, Minas Gerais. Brasil. 35.400-000.
E-mail: anavolp@gmail.com
Recibido: 19-IV-2015.
Aceptado: 13-V-2015.
060_9135 El consumo de pulpa.indd 931 11/07/15 00:10
932 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
However, the skinfold thickness (p = 0.018) and total body
fat (p = 0.016) decreased in overweight women. There was
reduction of total protein (p = 0.049) due to the globulin
reduction (p = 0.005), but the nutritional status was main-
tained in eutrophic group.
Conclusion: the intake of 200g acai pulp, modulated
the EGF and PAI-1 expression, possibly by modulation
of acai on the parameters of body composition, dietary,
clinical, biochemical and inflammatory, led to a redistri-
bution and resizing of body fat of the trunk area, and
presumably increased visceral fat.
(Nutr Hosp. 2015;32:931-945)
DOI:10.3305/nh.2015.32.2.9135
Key words: Obesity. Inflammation. Plasminogen activa-
tor inhibitor-1. Epidermal growth factor. Acai.
peso. Hubo una reducción de la proteína total (p = 0,049)
debida a la disminución de globulina (p = 0,005), pero el
estado nutricional se mantuvo en el grupo eutrófico.
Conclusión: la ingesta de 200 g de pulpa de acai mo-
dula el EGF y PAI-1 de expresión, posiblemente por la
modulación del acai en los parámetros de la composición
corporal, la dieta, clínicos, bioquímicos e inflamatorios,
lo que dio lugar a una redistribución y modificación del
tamaño de la grasa corporal de la zona del tronco, y, pre-
sumiblemente, un aumento de la grasa visceral.
(Nutr Hosp. 2015;32:931-945)
DOI:10.3305/nh.2015.32.2.9135
Palabras clave: Obesidad. Inflamación. Inhibidor del ac-
tivador del plasminógeno-1. Factor de crecimiento epidér-
mico. Acai.
Abbreviations
% BF: Body fat percentage
% TBF: Total body fat percentage
% TF: Truncal fat percentage
aMED: Score Alternative Mediterranean Diet Score
AC: Abdominal circumference
AFMI: Arm fat-muscle index
BI: Biceps Skinfold
BIA: Tetrapolar electrical bioimpedance
BMI: Body Mass Index
CD: Chronic diseases
EGF: Epidermal Growth Factor
ELISA: Enzyme linked immunosorbent assay
FFQ: Food Frequency Questionnaire
FRAP: Ferric Reducing Antioxidant Power
GLUT-4: Insulin-sensitive glucose transporter
HC: Hip circumference
HDL–c: High Density Lipoprotein cholesterol
HEI: Healthy Eating Index
HOMA-IR: Homeostatic model assessment of insu-
lin resistance
IL-1: Interleukin-1
IL-8: Interleukin-8
IQD-I: International Quality Diet Index
LDL–c: Low Density Lipoprotein cholesterol
MAPK: Mitogen activated protein kinase
METs: Metabolic equivalent units
NF-kB: Nuclear Transcription Factor Kappa Beta
DQI: Original Diet Quality
PAI-1: Plasminogen activator inhibitor-1
PDGF–AA: Platelet Derived Growth Factor
PI3-k: Phosphatidylinositol 3-kinase
PKB/AKT: Protein kinase –B
QUICKI: Quantitative insulin sensitivity check in-
dex
REE: Resting Energy expenditure
RFS: Recommended food score
SUB: Subscapular Skinfold
SUPR: Supra-iliac Skinfold
TEAC: Trolox equivalent antioxidant capacity
TFEQ: Three Factor Eating Questionnaire
TNF-α: Tumor Necrosis Factor-α
TRI: Triceps Skinfold
TUA: Total upper arm area
UAC: Upper arm circumference
UAMC: Upper arm muscle circumference
UFA: Upper arm fat area
UMA: Upper arm muscle area
UMAc: Corrected upper arm muscle area
VEGF: Vascular Endothelial Growth Factor
WC: Waist circumference
WHR: Waist-hip ratio
Introduction
The obesity is considered a complex disease of
multifactorial and endemic etiology. Its clinical fea-
ture is associated with increased morbidity and mor-
tality by chronic diseases (CD), such as: diabetes type
2, hypertension and cardiovascular disease. The as-
sumption that the metabolic changes lead to adiposity
excess is essential to extensively studied hypothesis
that the distribution of body fat, as well as truncal
and or visceral fat increase, seems to be related to the
CD, and the main link involves oxidative and inflam-
matory state1,2.
As a result, there are evidences that a higher level of
oxidative stress in obese is an important factor which
relates to the increase of the inflammatory process
and the modification of endothelial function, leading
to a state of low-grade chronic inflammation2, accom-
panied by the expression of markers of coagulation
cascade and growth factors; quoting the plasminogen
activator inhibitor-1 (PAI-1), which in situations of
larger adiposity is released by adipocytes performing
the function of physiological inhibitor of fibrinolysis,
being able to lead the formation of thrombi3, the fibri-
nogen, as an acute phase reactant protein, in response
to inflammation, may accelerate the formation of these
clots/thrombus4.
060_9135 El consumo de pulpa.indd 932 11/07/15 00:10
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Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
Together, the growth factors can participate of
this inflammatory process. The vascular endothe-
lial growth factor (VEGF) induced by endothelial
cells and inflammatory cytokines, interleukin-1 (IL-
1), interleukin-8 (IL-8) and tumor necrosis factor
(TNF-α), is a major regulator of angiogenesis and
repair of the lesions generated by the inflammation5.
As the platelet derived growth factor (PDGF-AA),
the transforming growth factor-alpha (TGF-α) and
epidermal growth factor (EGF) released by inflam-
matory cells and the endothelium exercise chemoat-
tractant functions for the local endothelium and con-
sequent repair of this process. However, the growth
factors determine endothelial functions and data in
the literature of how they protect the endothelium or
promote CD are still insufficient6.
Studies reported that high levels of PAI-1 in plasma
are influenced by age, gender, obesity, hypertension,
smoking, hypercholesterolemia, dietary patterns, and
genetic polymorphisms, and suggested that the vis-
ceral adipose tissue, this marker is differentiated to
provide more information about the fibrinolytic sta-
te7,8. The plasma fibrinogen has been identified as a
cardiovascular risk factor, their concentrations have
been associated with body mass index (BMI), waist
circumference (WC), hip circumference (HC), fas-
ting glucose, blood insulin, HDL -cholesterol, systo-
lic and diastolic blood pressure8,9. Few studies have
reported that higher plasma VEGF concentration in
obese patients, and its relation to the distribution of
fat remains unclear. However, their concentrations
are associated with the increased BMI, progression
of atherosclerosis, low HDL-c, hypertriglyceride-
mia, systolic pressure and hyperglycemia10.
Current researches point the EGF and its inver-
se correlation with concentrations of fasting gluco-
se, insulin and HOMA-IR index. Its concentration
is also proportional to the increase in adiposity;
however there is not relationship between EGF with
BMI11.
The modulation of the mechanisms involved in
inflammation, by the diet, is highlighted by the pro-
tective effect to CD2. Several effects of interventions
with fruits, rich in flavonoids, have been found to
inflammatory biomarkers. It was observed a reduc-
tion in PAI-1, fibrinogen and VEGF in patients with
overweight or comorbidities12,13,14. In healthy sub-
jects, other studies point the reduction of EGF, PAI-
113 and fibrinogen15.
The beneficial effect of fruits and dietary pattern in
the improvement of the inflammatory status is alre-
ady well understood13. In fact, fruits increase the an-
tioxidant capacity in plasma. Among the eleven most
consumed fruits in Brazil, recent studies suggest the
acai as the main responsible for the increase in the
daily intake of phenolic compounds, flavonoids and
total antioxidant capacity13,16. Mertens-Talcott and
colleagues (2008) demonstrated that consumption of
acai pulp tripled the plasma antioxidant capacity16.
In view of its potential of nutritional utilization and
due to its relevance in Brazilian dietary consumption,
in this study, it was given importance to Acai berry
due to its antioxidant properties and modulation of
endothelial homeostasis. No studies in the literature
presenting its action on markers of endothelial dys-
function17.
Due to the paucity of studies in the literature, this
study will allow us to verify by the first time in hu-
mans, the effect of acai on the endothelial injury mar-
kers and their relationship with anthropometric, body
composition, dietetic and inflammatory parameters,
since it was known that the obesity leads to endothe-
lial dysfunction. So, the acai can modulate the inflam-
matory profile, protecting the endothelial damage and
reducing the risk of cardiovascular disease through
its antioxidant properties. In this view, the objective
of this study was to investigate if the consumption of
200g acai pulp has an effect on inflammatory mar-
kers of fibrinolytic cascade (PAI-1 and fibrinogen)
and growth factors (EGF, TGF-α and PDGF-AA and
VEGF), and also, on the anthropometric, body com-
position, clinical and biochemical parameters in heal-
thy women.
Methods
Study sample
This is a nutritional intervention, self-controlled
involving women aged between 18 and 35 and BMI
determined between 27 - 35 kg/m2 for the group 2
(overweight and obesity class I and II) and 18.5 - 25
kg/m2 for group 1.
It were excluded: women who could not read or
write, who had more than 10% of body weight change
before the beginning of the study, as well as, blood
pressure > 130/85 mmHg, fasting glucose > 100 mg/dl,
dyslipidemia history, total cholesterol > 200mg/dl or
triglycerides > 150 mg/dl, allergies, eating disorders
and/or acai intolerance. It were also excluded women
who had special diets (vegetarian diet, Atkins diet,
etc.), who were taking nutritional supplements (vita-
min complex , minerals) or chronic medication (ex-
cept contraceptives), women who were top athletes or
had acute chronic diseases, infectious, inflammatory,
as well as, pregnant or breastfeeding, smokers and
were classified at the Three Factor Eating Question-
naire - TFEQ18 which assess the restriction, disinhi-
bition and hunger with low scores: 0-5; 0-9; 0-4; and
high: ≥ 10; ≥ 13; ≥ 8. The omitted cases were discussed
in group with the study coordinator (ACPV).
Experimental design
The study was conducted during 4 weeks and divi-
ded in 3 steps (Figure 1).
060_9135 El consumo de pulpa.indd 933 11/07/15 00:10
934 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
Anthropometric and body composition parameters
The body weight was measured using a Welmy® di-
gital scale (model W200-A); the height was evaluated
by a vertical stadiometer coupled to the scale, with 2.00
m long, divided into centimeters and subdivided into
millimeters (1 mm of precision)19,20. The BMI was cal-
culated by means of weight and height in order to group
the women into normal weight and overweight group.
It were measured the waist circumference (WC), hip
circumference (HC), abdominal circumference (AC)
and upper arm circumference (UAC) with a flexible
and inelastic metric tape, divided into centimeters and
subdivided into millimeters (accuracy of 1 mm)21,22.
The thickness of the subcutaneous tissue was
analyzed by measuring the following skinfolds: triceps
(TRI), biceps (BI), subscapular (SUB), supra-iliac
(SUPR), and the sum of them was used to calculate the
percentage of total body fat (%TBF)23. All skinfolds
and circumferences were performed in triplicate and
the mean of three measurements was considered.
The sum of skinfolds; the total upper arm area
(TUA); upper arm muscle area corrected for women
(UMAc); upper arm muscle circumference (UAMC);
upper arm fat area (UFA); truncal fat percentage
(%TF); were calculated using the circumference and
skinfold measures. Body composition represented by
body fat variables (kg), fat-free mass (kg), body fat
percentage (%BF) and the resting energy expenditu-
re (REE; Kcal) were determined by horizontal tetra-
polar bioelectrical impedance (Biodynamics, model
310e)22,23.
Clinical and biochemical parameters
The systolic and diastolic blood pressure were perfor-
med in triplicate following a 5 minute interval between
measurements by means of a Omron® pressure apparatus
(model HEM-705CP) positioned on the right arm of the
women volunteer which were sitting at rest24.
In order to quantify the physical activity value, it was
used an activities of different intensities scale, in 24-hour
period. After, they were converted into equivalent meta-
bolic units (METs)25.
The extraction of blood samples was performed af-
ter 12 hours of fasting by a trained pharmaceutical. One
blood sample was extract of each volunteer: two serum
tubes (5 mL each) and four tubes containing EDTA for
plasma (4 mL). One of the 5 mL tubes and a serum sam-
ple of 1 mL of EDTA to plasma were sent for bioche-
mical analysis (fasting glucose, insulin, total cholesterol
and lipoproteins, triacylglycerols and total proteins).
The fasting glucose, total cholesterol and high density
lipoprotein cholesterol (HDL-c) were determined by en-
zymatic colorimetric method (Metrolab® spectrophoto-
meter, model 2800). Low density lipoprotein cholesterol
(LDL-c) concentrations were calculated according to the
Friedewald et al. (1972) equation: LDL-c = total choles-
terol - HDL-c - (Triacylglycerols/5), for samples which
showed result of triglycerides < 400 mg/dL. Total prote-
ins were determined by Biuret-colorimetric method and
albumin by green- colorimetric of bromocreso (Metro-
lab® spectrophotometer, model 2800) with commercially
available specific kits (Bioclin, Quibasa). The dosage of
globulin was determined by subtracting the amount of to-
Fig. 1.—Study
design.
060_9135 El consumo de pulpa.indd 934 11/07/15 00:10
935
Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
tal protein and albumin - the albumin/globulin ratio. The
dosage of total proteins was performed in order to mo-
nitoring the nutritional status of the volunteers. To dose
fasting insulin, it was used the Access Ultrasensitive In-
sulin test (Acess® Immunoassay System), determined by
chemiluminescence immunoassay. In chemiluminescent
immunoassay, it was used the protocol provided by the
manufacturer. The kit detection sensitivity was 0.3 μIU/
mL and precision of < 10% variation coefficient (VC).
The results were expressed as μIU/mL.
To determine the insulin sensitivity, the HOMA-IR
(model assessment of insulin sensitivity homeosta-
sis) was determined by the following formula: HO-
MA-IR = [Insulin (μU/L) X glucose (mmol/L)/22.5] . To
determine the functional capacity of the pancreatic beta
cells, the HOMA beta formula was used: [20 X insulin
(μU/L)/(glucose (mmol/L) -3.5)]26.
Serum concentrations of PAI-1, fibrinogen, VEGF,
EGF, TGF-α and PDGF-AA were determined by En-
zyme linked immunosorbent assay (ELISA), using MI-
LLIPLEX® MAP specific commercial kits (Millipore
Corporation, Billerica, MA, USA) with a sensitivity 2.8
pg/mL to EGF; 0.8 pg/mL to TGF-α; 0.4 pg/mL to PD-
GF-AA; 26.3 pg/mL to VEGF; 4.8 pg/mL to PAI-1 and
0,004ng/mL to fibrinogen. The PAI-1/body fat (kg) in-
dex were calculated through the PAI-1 marker and body
fat (kg).
Dietary parameters
Calories, protein, carbohydrates, lipids, fatty acids:
satured, monounsaturated, polyunsaturated, trans, ome-
ga-3, omega-6, omega-9, (omega-3/omega-6) ratio, total
fiber (g) and cholesterol (mg) were calculated. The acai
pulp has been added to the FFQ, adopting the nutritional
composition of the label of acai pulp. Acai pulp (100g)
contains: 70 calories, 3g of carbohydrates, 2 g of protein,
5 g of total fat, 1 g of saturated fat and 3g of dietary fiber.
To evaluate the diet quality, the amount of the food
registered as household measures, in Food Frequency
Questionnaire (FFQ), was converted in grams of food/
day and, later, in portions to calculate the Original Diet
Quality Index (DQI)27; the International Quality Diet
Index (IDQ-I)28; the Healthy Eating Index (HEI)29; the
alternative Mediterranean Diet Score (aMED Score)30
and the Recommended Food Score (RFS)31. The dietary
antioxidant capacity was also calculated by means of
comparing tables containing values of Ferric Reducing
Antioxidant Power (FRAP), the antioxidant content of
each food present in the FFQ. The table information re-
ferred a portion of 100 g of food represented by two pa-
rameters to assess the antioxidant capacity: values of Fe-
rric Reducing Antioxidant Power (FRAP). Through the
portion of each food consumed by volunteers before and
after acai consumption, were obtained as the proportion
of the FRAP values representing its antioxidant content.
Data analysis
The data were presented as mean ± standard deviation
for those variables that fit in a normal distribution, or
median and interquartile range for the variables that did
not fit in a normal distribution. We used the Kolmogo-
rof-Smirnov normality test to check these settings. In ad-
dition, the Student t test and Wilcoxon, both paired, were
performed to evaluate the intervention effect by BMI.
Comparisons between the baseline mean and median
of groups were made by Student t-test (parametric) and
U-Mann-Whitney (non-parametric). For all statistical
tests, we adopted a significance level of 5%. Statistical
analysis were performed using SPSS version 17.0 Sta-
tistics software.
Results and discussion
The average age of the eutrophic group was
23.58 ± 0.66 and of overweight group was 24.27 ± 0.98.
In the basal state, the anthropometric variables in the
overweight group were increased compared to the eu-
Fig. 2.—Selection
scheme of volun-
teers.
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936 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
Table I
Anthropometric and body composition characteristics before and after the consumption of acai pulp
TOTAL (n=40) EUTROPHICS (n=24) OVERWEIGT (n=15)
T0T1∆ paT0T1∆ paT0T1∆ papb
Body weigt kg 61.55
(55.12-77.00) 61.45
(56.00-77.70) -0.10 0.076 57.86±5.54 58.26±5.50 0.40 0.031 80.32±11.53 80.40 ±11.12 0.08 0.866 <0.001
BMI, kg/m222.71
(20.91-27.43) 23.17
(21.07-27.51) 0.46 0.065 21.52±1.56 21.68±1.59 0.16 0.028 29.36 ± 2.75 29.38 ±2.70 0.02 0.890 <0.001
Upper arm
circumference,
cm
28.33
(26.53-31.90) 28.33
(26.17-31.75) 00.025 27.00±1.56 26.80±1.95 -0.20 0.157 32.50 ±2.27 32.03 ±2.29 -0.47 0.136 <0.001
Waist
circumference,
cm
73.00
(68.85-81.45) 72.50
(68.25-79.53) -0.50 0.147 69,87±3,30 69,78±1,95 -0,09 0.769 84.81±6.96 84.10 ±6.88 -0.71 0.129 <0.001
Abdominal
circumference,
cm 84.99± 10.09 84.02± 9.76 -0.97 0.045 70.07±5.27 78.2±4.89 8.13 0.130 90.80
(88.53- 104.00) 91.76
(88.00-95.66) 0.96 0.256 <0.001
Hip
circumference,
cm
98.70
(94.00-110.45) 100.00
(95.65-109.09) 1.30 0.767 97.24±5.29 97.36±4.38 0.12 0.870 113.33 ±8.86 113.25±8.29 -0.08 0.884 <0.001
Triceps skinfold,
mm 22.50± 6.25 21.49±5.73 -1.01 0.013 19.52±4.22 18.80±4.14 -0.72 0.181 27.47 ± 6.01 25.98 ± 5.24 -1.49 0.018 <0.001
Biceps skinfold,
mm 11.44
(8.44-16.78) 10.70
(8.40-13.89) -0.74 0.005 10.1
(7.56-11.70) 9,06
(7.65-11.21) -1.04 0.253 17.20±4.63 16.21 ±5.56 -0.99 0.045 <0.001
Subscapular
skinfold, mm 19.99±7.18 19.89±6.62 -0.10 0.823 16.15±4.41 16.28±4.51 0.13 0.812 26.39 ±6.33 25.92 ±5.00 -0.46 0.553 <0.001
Supra-iliac
skinfold, mm 22.34±7.97 22.52± 6.90 0.18 0.694 17.70±4.85 18.86±5.42 1.16 0.046 30.08±5.83 28.69 ±4.123 -1.39 0.054 <0.001
Skinfolds, mm 77.78± 23.09 75.99±20.98 -1.79 0.103 63.76±12.76 63.49±13.13 -0.27 0.846 101.15 ±16.42 96.82 ±13.71 -4.33 0.018 <0.001
060_9135 El consumo de pulpa.indd 936 11/07/15 00:10
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Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
Table I (cont.)
Anthropometric and body composition characteristics before and after the consumption of acai pulp
TOTAL (n=40) EUTROPHICS (n=24) OVERWEIGT (n=15)
T0T1∆ paT0T1∆ paT0T1∆ papb
Upper arm
muscle 20.78±23.09 20.99± 20.98 0.21 0.917 20.86±1.34 20.89±1.38 0.03 0.866 23.87 ±1.73 23.86 ±1.71 -0.01 0.978 <0.001
Upper arm total
area, cm263.91
(56.02-81.02) 63.88
(54.52-80.21) -0.03 0.024 57.58
(54.34-60.76) 55.88
(52.08-63.88) -1.70 0.072 84.47±11.91 82.03 ±12.03 -2.44 0.153 <0.001
Corrected upper
arm muscle area,
cm232.33± 7.46 32.39± 7.48 0.06 0.919 28.28±4.36 28.39±4.57 0.11 0.857 39.08 ±6.66 39.04 ±6.64 -0.04 0.974 <0.001
Upper arm fat
area, cm235.75± 10.56 34.28± 9.69 -1.47 0.008 29.97±5.91 29.07±5.85 -0.90 0.145 45.38± 9.57 42.98 ±8.56 -2.40 0.023 <0.001
Truncal fat, % 54.80
(51.65-58.60) 57.34
(50.89-59.32) 2.54 0.001 53.02
(50.0-58.2) 55.34
(50.78-59.19) 2.32 0.003 55.59
(53.04-59.106) 57.44
(54.69-59.410) 1.85 0.191 0.119
Body fat
(formula*)% 34.15± 0.70 33.94±0.67 -0.21 0.371 31.54±3.17 31.58±3.31 0.04 0.911 38.49 ±2.47 37.88± 2.17 -0.61 0.016 <0.001
Body fat (BIA),
kg 18.60
(15.62-26.17) 19.30
(16.32-25.17) 0.70 0.190 16.73±3.17 16.70±2.99 -0.03 0.029 30.20
(24.80-35.40) 28.50
(24.20-35.50) -1.70 0.589 <0.001
Fat-free mass
(BIA), kg 44.67±6.96 44.61±6.78 -0.06 0.687 39.90
(38.45-44.05) 40.00
(38.90-43.65) 0.10 0.951 50.68 ±6.98 50.50 ±6.80 -0.18 0.474 <0.001
Body fat (BIA), % 31.79±5.26 32.17±5.12 0.38 0.105 28.82±3.62 29.38±3.24 0.56 0.092 36.74 ±3.568 36.82 ±4.23 0.08 0.804 <0.001
REE, kcal 1331.50
(1180.75-1518.75) 1323.00
(1202.75-1508.25) -8.0 0.706 1212,00
(1169.50-1342.00) 1217,00
(1183.00-1327.00) 5.0 0.951 1542.33 ±210.44 1535.60 ±206.32 -6.73 0.389 <0.001
T0 : Baseline characteristics (before the intervention). T1 : Final characteristics (after the intervention). ∆: Delta, difference between final and initial period (∆= T1 –T0 ). REE: Resting Energy expenditure.
Presented data: mean± standard deviation or median (Q1-Q3) as parametria. Normality test: Kolmogorov- Smirnov, p<0.05.
*Body Fat as calculated from sum of 4 skinfolds (tríceps, bíceps, supra-iliac and subscapular).
*a Paired Student t Test or Paired Wilcoxon Test.
*b Student t Test or U-Mann- Whitney, for comparison between groups before the acai intake.
060_9135 El consumo de pulpa.indd 937 11/07/15 00:10
938 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
trophic group. It was expected, since BMI quantifies
the level of body fat considering the body weight of
the individual. However, the truncal fat was indifferent
between the groups, which could be expected, because
BMI is related to fat-free mass, which impede the dis-
tinction of the local where the fat is located, either the
muscle amount of the individual. So eutrophic indivi-
duals can present similar or greater change in truncal fat
than overweight individuals19,33.
The anthropometric assessment enabled the detec-
tion of changes in nutritional status and body compo-
sition mediated by acai consumption. In all volunteers
there was a reduction of AC,TRI, BI, TUA, UFA and a
considerable increase in truncal fat, however, without
changing in food pattern, REE or METs. These results
suggest a redefinition of body fat in all volunteers with
accumulation in the truncal region and decrease in pe-
ripheral areas of the upper limbs, with a possible reduc-
tion of subcutaneous fat and considerable increase in
visceral fat. In this study there was no measurement of
body fat for invasive methods of dual energy absorp-
tion of the conventional X-ray (DEXA) which would
allow better evaluation of these parameters. However, it
is known that truncal fat reflects an accumulation of fat
in the intra-abdominal or visceral cavity, including sub-
cutaneous routes and intermuscular fat throughout the
fat deposits region of the trunk, in addition to epicardial
and pelvic deposits34.
In eutrophic group, the acai consumption focused on
weight gain, BMI, supra-iliac skinfold, truncal fat per-
centage and reduction in body fat (kg). These results
possibly show a fat redistribution with increased vis-
ceral subcutaneous or intramyocellular due their high
relationship with truncal fat alteration35,36. The fat re-
distribution is directly related to inflammatory markers
concentration. Raji et al. (2001) showed that individuals
with greater accumulation of abdominal fat had grea-
ter relationship between PAI-1 concentrations and de-
position of abdominal fat: abdominal (r = 0.7), visceral
(r = 0.62), subcutaneous (0, 46) (p < 0.01)37.
In the overweight group, there was a significant re-
duction in triceps skinfold, biceps skinfold, sum of skin-
folds, upper arm fat area and total body fat. The changes
of anthropometric measurements and skinfolds repre-
sented a reduction in subcutaneous fat. Nevertheless,
visceral adipose tissue was not sensitive to modifica-
tion. Moreover, the reduction in skinfold measures and
the upper arm fat area are closely related to the amount
of adipose tissue in the body, thus the decrease of these
anthropometric parameters presumably is directly rela-
ted to the reduction of total fat percentage36,38. We eva-
luated the muscle mass of the volunteers by means of
the adequacy of UAC and TRI measures. Eutrophic and
overweight volunteers were classified as obese. Howe-
ver, after adjustment of the UAMC, the two groups were
classified as normal. These results demonstrate that the
muscle mass was preserved in both groups.
The biochemical and clinical data, before the inter-
vention with acai, were within the normal range. These
results were expected, because this normality was inter-
posed the inclusion criteria of the study. However for
those with overweight it was observed a higher HO-
MA-IR, SBP and DBP when compared to eutrophic
group. The decrease in blood pressure is, possibly, co-
rrelated with a decrease in body fat and consequent re-
duction in the risk of developing cardiovascular disease.
Lavie et al (2003) suggested that the high percentage
of body fat, estimated by skinfold measurements, can
be an independent predictor of cardiovascular death by
increased pressure39.
As noted, the overweight group presented reduction
of fat percentage, skinfolds and remained with a lipid,
glicidic and insulin homeostasis even if at baseline had
higher HOMA-IR, and the maintenance has been sus-
tained after acai consumption. This homeostasis preser-
vation was due to the good overall clinical status of the
participants and, possibly, by the positive impact of acai
pulp consumption, since the volunteers kept their eating
pattern, the total antioxidant capacity of the diet and le-
vel of physical activity.
Udani et al. (2011) in its pilot study, performed with
overweight individuals in homeostasis, who consumed,
for 4 weeks, 200g of acai pulp, it was observed signifi-
cant reduction in total cholesterol, fasting glucose and
insulin, in addition to the blood pressure maintenan-
ce, however such volunteers received a brochure with
orientation to avoid foods that contained nitrates (eg.
bacon and hot dogs), which could have contributed to
these results40.
Other intervention works with fruits rich in anthocya-
nins reinforce our results. Basu et al (2010) showed that
the use of blueberry reduced the systolic and diastolic
blood pressure by about 6% and 4%, respectively, in in-
dividuals with metabolic syndrome41. In healthy human
or with any cardiovascular risk factor there was a reduc-
tion in systolic and diastolic blood pressure after supple-
mentation with blueberries42. Another study conducted
with acai extract (injections of 10 to 100 mg extract)
in rats showed that acai had a endothelium dependent
vasodilator effect due to the effects on the nitric oxide
production17.
We found that the total protein - an important mar-
ker of nutritional status - were reduced after the inter-
vention with acai, as verified for the total and eutrophic
group, and the reduction of globulin in greater magni-
tude caused the increase of the albumin/globulin ratio,
but the values remained within the reference values and
without affecting the muscle reserves. So, all the volun-
teers kept their nutritional condition. At the same time,
albumin is an indication of the diet protein content, and
it refers to inflammatory processes, therefore there is a
reverse correlation between the concentrations of albu-
min and globulin as a compensatory mechanism, in or-
der to maintain the total protein level and blood oncotic
pressure43.
In relation to eutrophic voluntary, the isolated in-
crease in serum albumin supposedly correlates with its
carrier function of free fatty acids. The increase in trun-
060_9135 El consumo de pulpa.indd 938 11/07/15 00:10
939
Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
cal fat percentage of this group is directly related to the
visceral fat increase, and the literature addresses the vis-
ceral adipose tissue (VAT), the most active, sensitive to
lipolysis and more resistant to insulin action and allows
a higher concentration of free fatty acids (FFA), which
are carried by albumin directly to peripheral tissues for
storage or as an energy source. Thus a possible likely
explanation for this isolated increase can be related to
its transport function35,36.
In view of the inflammatory markers production PAI-
1 and fibrinogen and growth factors (EGF, TGF-α, PD-
GF-AA and VEGF) dependent of the oxidative stress
increase and endothelial inflammation mainly, the in-
flammatory profile before the acai consumption was not
different between eutrophic and overweight volunteers.
The effect of the intervention (consumption of 200g
of acai) in free-living context, during four weeks,
showed just alteration on the PAI-1 increase in all vo-
lunteers and EGF and PAI-1 alteration in the overweight
group. The isolated increase of PAI-1 can be inter-rela-
ted to PAI-1 changes in the overweight group, conco-
mitant with this fact, another supposed explanation is
related to the increase in truncal fat evidenced by the
total group. Studies indicated that an increase a truncal
fat is associated with PAI-1 increase. Together with the
truncal fat increase, there is an increase mobilization of
non-esterified fatty acids which stimulates the adipo-
cyte secretion of PAI-144.
Likewise, the PAI-1/BF ratio, in all volunteers
(0.039) and in the overweight group (0.019) supports
the hypothesis of PAI-1isolated increased, since its in-
crease was independent of body fat in total or overwei-
ght group44. The PAI-1 change can be influenced by
several factors of anthropometry, clinical, biochemical
Fig. 3.—Representa-
tion of the concentra-
tion of EGF marker in
plasma. Total (n=30);
eutrophic (n=21) and
overweight (n=9).
Teste t-Student (mean)
or *Wilcoxon paired
(median), (p<0,05).
0,0 TOTAL EUTROPHIC OVERWEIGT
*P=0,021
EGF concentration before the açaí consumption
EGF concentration after the açaí consumption
*P=0,940
*P=0,315
mean or median of the concentration s of EGF (pg/mL) in the plasma
10,0
20,0
30,0
40,0
Fig. 4.—Representation of
the concentration of PAI-1
marker in plasma. Total
(n=37); eutrophic (n=23)
and overweight (n=14).
Teste t-Student (mean) or
*Wilcoxon paired (me-
dian), (p<0,05).
0,0
2,0
4,0
6,0
8,0
10,0
12,0
14,0
16,0
TOTAL EUTROPHIC OVERWEIGT
P=0,011
PAI-1 concentration before the açaí consumption
PAI-1 concentration after the açaí consumption
P=0,140
P=0,016
mean or median of the concentration s of PAI-1 (Ug/mL) in the plasma
060_9135 El consumo de pulpa.indd 939 11/07/15 00:11
940 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
Table II
Biochemical and clinical characteristics before and after the consumption of acai pulp
TOTAL (n=40) EUTROPHIC (n=25) OVERWEIGT (n=15)
T0T1∆Pa T0T1∆Pa T0T1∆ papb
Glucose, mg/dl 77.50
(75.00-83.50) 78.00
(75.00-84.00) 0.50 0.771 79.28±6.44 78.08±5.04 -1.20 0.250 77.00
(75.00-80.00) 83.00
(76.00-90.00) 6.00 0.421 0.911
Insulin** 5.68
(4.40-7.56) 6.17
(4.05-8.02) 0.49 0.868 5.34
(4.40-6.40) 6.00
(4.05-8.49) 0.66 0.737 7.12 ±2.45 6.67 ±3.16 -0.45 0.613 0.144
HOMA-IR** 1.23
(0.88-1.61) 1.15
(0.73-1.64) -0.08 0.412 1.05
(0.87-1.28) 1.17
(0.77-1.64) 0.12 0.798 1.48 ±0.56 1.25 ±0.65 -0.23 0.230 0.044
HOMA-b** 133.19
(108.33-189.38) 125,12
(86.31-189.80) -8.07 0.989 128.00
(102.27-169.13) 146.80
(97.71-206.36) 18.80 0.088 157.68
(115.78-199.80) 94.75
(73.05-161.15) -62.93 0.125 0.214
QUICK 0.37
(0.35-0.39) 0.37
(0.35-0.40) 0 0.085 0.38
(0.36-0.39) 0.37
(0.35-0.41) -0.01 0.427 0.36 ±0.02 0.38 ±0.03 0.02 0.063 0.234
Total proteins,
g/dl 7.05
(6.62-7.67) 7.00
(6.25-7.30) -0.05 0.048 7.27±0.55 7.06±0.46 -0.21 0.049 6.96 ±0.58 6.72 ±0.80 -0.24 0.295 0.101
Albumin, g /dl 3.75±0.30 3.84±0.45 0.09 0.263 3.73±0.29 3.89±0.32 0.16 0.008 3.78 ±0.31 3.75 ±0.61 -0.03 0.888 0.660
Globulin, g/dl 3.60
(2.82-3.80) 3.15
(2.42-3.70) -0.45 0.007 3.54±0.57 3.17±0.65 -0.37 0.005 3.40
(2.40-3.70) 2.90
(2.30-3.60) -0.50 0.244 0.130
Albumin/globu-
lin ratio 1.03
(0.94-1.37) 1.20
(0.90-1.59) 0.17 0.006 1.08±0.23 1.29±0.37 0.21 0.001 1.08
(0.97-1.62) 1.14
(0.94-1.81) 0.06 0.349 0.150
Cholesterol,
mg/dl 188.46 ±34.00 188.27 ±38.29 -0.19 0.964 184.56±29.05 184.72±32.99 0.16 0.977 194.96 ±41.26 194.20 ±46.45 -0.76 0.897 0.356
Triacilglicerol,
mg/dl 79.94±35.85 81.32±35.44 1.38 0.760 70.00
(56.00-84.00) 71.00
(50.50-88.00) 1.00 0.737 89.06 ±41.94 95.40 ±43.57 6.34 0.512 0.252
LDL, mg/dl 106.79±30.59 105.64±33.94 -1.15 0.753 102.30±27.82 101.12+31.13 -1.18 0.810 114.26 ±34.40 113.18 ±38.08 -1.08 0.845 0.236
HDL, mg/dl 65.00
(55.22-77.50) 66.00
(56.00-76.00) 1.00 0.723 67.20±14.41 69.12±14.41 1.92 0.232 63.06±12.03 61.66±12.38 -1.40 0.604 0.357
Systolic blood
pressure, mmHg 106.16
(95.58-115.00) 103.99
(93.41-112.91) -2.17 0.083 100.93±9.41 100.59±10.54 -0.34 0.856 118.00
(107.00-124.00) 107.66
(97.33-118.33) -10.34 0.013 <0.001
Diastolic blood
pressure, mmHg 74.16
(64.41-80.16) 71.16
(64.41-78.50) -3.00 0.202 70.33
(63.16-77.00) 67.00
(62.67-76.33) -3.33 0.786 76.66
(73.30-88.00) 75.00
(68.67-81.00) -1.66 0.096 0.009
Metabolic equi-
valent units/ day 39.35
(34.86-48.35) 38.57
(35.03-45.45) -0.78 0.886 39.50
(34.15-46.25) 38.00
(35.13-45.30) -1.50 0.904 39.20
(34.75-48.40) 40.27
(33.62-47.05) 1.07 0.875 0.342
T0 : Baseline characteristics (before the intervention). T1 : Final characteristics (after the intervention). ∆: Delta, difference between final and initial period (∆= T1 –T0 ).
HOMA-IR: Homeostatic model assessment of insulin resistance; HOMA-beta INDEX; QUICKI: Quantitative insulin sensitivity check index;LDLc: LDL Cholesterol; HDLc: HDL Cholesterol.
Presented data: mean± standard deviation or median (Q1-Q3) as parametria. Normality test: Kolmogorov- Smirnov, p<0.05.
*a Paired Student t Test or Paired Wilcoxon Test. *b Student t Test or U-Mann- Whitney, for comparison between groups before the acai intake. ** n= 37: 26 eutrophic and 11 overweight.
060_9135 El consumo de pulpa.indd 940 11/07/15 00:11
941
Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
or even inflammatory changes, which acted jointly or
individually. Among them, the body composition is a
very sensitive determinant to the inflammatory mar-
kers changes.
Therefore, another possible modulation of PAI-1
could be justified by an increase in baseline HOMA-IR
in overweight group associated with an increase insu-
lin resistance; however, they are lower concentrations
to supposed values for developing diabetes type 2. As
reported in the literature, in states of bigger insulin re-
sistance and inflammation, the plasma membrane of
adipocytes express EGF receptors, which by means
of intracellular signaling increase the binding of EGF
binding. These phosphorylated sites give the acti-
vation of different proteins, such as: Grb2, Shc, Src
family tyrosine kinases, PI3 kinase, and phospholipa-
se. Even as the insulin, some studies indicate that its
impaired signaling, in cells with increased resistance
to insulin, EGF increases the tyrosine phosphoryla-
tion and activation of the IRS-1 and IRS-2, which
enhances translocation induced by EGF and GLUT4
in the plasma membranes and possible stimulation of
glucose uptake in target tissues45. At the same time,
the increase of EGF is likely to change that media-
tes the PAI-1 increase in the overweight group. By
means of the binding of EGF to its receptor (EGFR)
with high affinity in cell surface, triggering the dime-
rization and phosphorylation each other through their
tyrosine kinase activity. Phosphorylated receptors can
initiate signal transduction, including MAPK, Akt and
JNK,AP-145. Thus, in the vasculature, the AP-1 trans-
duction, mediates not only the cell growth, but also the
gene expression of prothrombotic factor, pro-fibrotic,
PAI-1 in response to various stimuli3. Therefore, under
certain concentrations, the growth factor can be acting
on behalf of the process by improving the effective-
ness of insulin, at the same time, interceding in gene
production of PAI-1 by activating the same signaling
pathways that lead to their expression. However, the
literature that addresses these mechanisms does not
report the magnitude of change of the growth factor
concentrations, which leading to activation of this pro-
cess. All these tests were conducted only in vitro.
Thus, the acai effect was possibly performed by the
action of its cellular protection properties. The acai is
rich in anthocyanins which are a class of flavonoids
derived from polyphenols and according to Noratto et
al. (2011) the polyphenols action on the cellular pro-
tection is indirect, by act on the inhibition of protein
kinase C (PKC) and Mitogen activated protein kinase
(MAPK)46. The inhibition of these enzymes reduces
the binding ability of transcription factors, such as:
NF-kB or activator protein-1 (AP-1) to DNA and PAI-
1 expression rate is controlled. Thereby, the acai con-
sumption in this study, supposedly held its attenuation
effect, controlling the increase in gene expression of
PAI-1 to lower concentrations that could lead to their
pro-thrombotic action. However, we know that studies
that confirm the PAI-1 increase relates them to the for-
mation of thrombi in endothelial wall, also increasing
the risk of cardiovascular events and due to the rela-
tively low increase and very below of the reference
limits presented in the literature (5.0 to 40 ug/ml), was
not considered malefic. It was just a consequence of
the EGF increase that by means of cellular mechanis-
ms may have effected an improvement in glucose up-
take in the overweight voluntary46,47,48. So far, it was
not found in the literature intervention studies with
acai in humans, in free-living situation, which assess
the effect of this fruit on PAI-1, EGF, neither, on our
other evaluated markers. The studies which approach
this subject are often performed in vitro or with other
types of fruit.
In contradiction to our studies, in an intervention
study with cherry, oriented individuals for limiting
other fruits rich in polyphenols (tea, wine, berries)
besides the cherry itself (except those supplied by
the study) during 28 days, led to EGF and PAI-1 re-
duction. In this study, these decreases were related to
the cardiovascular disease, cancer and inflammation
reduction. However, in the weeks after the cherry
consumption, there was a minimal increase of PAI-1,
and the authors attributed this change to the residual
effects left after the cherry consumption, which atte-
nuated its increase. In this study, several other markers
reduction in the intervening period, did not demons-
trate the possibility of EGF to modulate PAI-1, since
in inflammation, a number of mediators are associated
in cytokines cascade promoting or reducing their se-
cretions13.
In other intervention study with following diets:
low-fat, high-fat diet and high fat supplemented with
20% of lingonberry, blackcurrant, blueberry, raspbe-
rry, acai, cranberry, plum or blackberry, for 13 weeks,
there was an increase in PAI-1 concentration, in rats
that received acai compared to other groups who re-
ceived other fruits. So, it must evaluate and consider
the mechanisms underlying of these effects, in view
of the optimal dose quantity, administration time and
even the reproducibility in humans49.
It is not possible to evaluate if the diet or some
specific compound of acai exerts direct action on the
markers changes or if the changes caused by diet on
the anthropometric, biochemical, clinical and inflam-
matory variables contributed to change these markers.
However this cause-effect study, has been the recog-
nition that dietary characteristics may have a decisive
influence on the inflammatory status and the dietary
patterns, that assess the quality of diet, may be asso-
ciated with deficiencies or to chronic diseases.
In relation to the total dietary antioxidant capacity,
there was no change after acai consumption, because,
possibly before the acai consumption, the volunteers
consumed foods (eg, fruits, juices and vegetables) rich
in other antioxidants as beta-carotene, lycopene, reti-
nol, ascorbic acid, tocopherols, zinc, selenium and co-
pper among others, replacing of the antioxidant effect
of acai anthocyanins.
060_9135 El consumo de pulpa.indd 941 11/07/15 00:11
942 Nutr Hosp. 2015;32(2):931-945 Izabelle de Sousa Pereira et al.
Table III
Diet characteristics before and after the consumption of açaí pulp
TOTAL (n=40) EUTRÓPHIC (n=25) OVERWEIGT (n=15)
T0T1∆ paT0T1∆ paT0T1∆ papb
Kcal 1980.43
(1673.67-2357.78) 1783.78
(1535.75-2606.98)-196.64 0.989 1881.62
(1680.34-2395.10) 1729.65
(1503.66-2354.96)-151.97 0.657 2040.60
(1470.90-2234.61) 2062.53
(1585.08-3324.53) 21.93 0.334 0.834
Protein, g 83.73
(67.22-114.06) 80.36
(68.92-110.97) -3.36 0.468 83.43
(69.96-111.06) 76.18
(67.85-96.92) -7.25 0.276 94.73±34.20 108.61±48.32 13.87 0.380 0.944
Lipids, g 65.62
(48.35-81.71) 62.01
(47.23-81.35) -3.61 1.000 68.69±22.37 63.85±19.97 -4.84 0.236 67.40±28.55 79.75±49.32 12.35 0.297 0.874
Cholesterol,
mg 270.18
(201.30-416.30) 268.14
(196.39-394.05) -2.03 0.648 265.38
(202.37-410.86) 243.09
(192.09-301.38) -22.29 0.158 328.61±167.94 396.77±228.47 68.15 0.408 0.542
Carboydrate, g 340.60
(235.35-564.30) 362.12
(258.93-689.49) 21.52 0.554 374.00
(264.24-589.77) 341.18
(237.63-558.44) -32.82 0.253 291.42
(231.48-346.48) 517.23
(288.95-937.79) 225.81 0.036 0.548
Omega-6 11.08
(7.36-14.22) 10.55
(6.87-14.38) -0.52 0.635 11.39
(7.52-13.44) 11.29
(7.41-13.48) -0.10 0.946 11.81±5.76 10.72±5.18 -1.09 0.368 0.791
Omega-3 1.186
(0.77-1.47) 1.10
(0.74-1.31) -0.08 0.219 1.17
(0.78-1.37) 1.12
(0.76-1.34) 9.95 0.778 1.18±0.48 1.04±0.33 -0.14 0.206 0.727
w-6/w3 ratio 9.69
(9.09-10.51) 9.64
(8.67-10.65) -0.05 0.933 9.62
(9.18-10.49) 9.67
(8.96-10.56) 0.05 0.345 9.67±1.77 9.95±2.33 0.28 0.386 0.461
RFS 10.00
(6.25-10.75) 9.00
(6.00-10.75) -1.00 0.118 8.68±2.32 8.24±2.50 -0.44 0.177 10.00
(6.00-11.00) 9.00
(5.00-11.00) -1.00 0.301 0.600
aMED score 4.50
(4.00-5.00) 5.00
(4.00-5.00) 0.50 0.839 3.00
(2.00-3.50) 2.00
(1.00-3.50) -1.00 0.163 5.00
(4.00-5.00) 4.00
(3.00-5.00) -1.00 0.793 0.503
HEI 3.00
(2.00-4.00) 2.00
(2.00-4.00) -1.00 0.594 74.10±10.55 74.58±7.62 0.48 0.803 3.00
(3.00-4.00) 2.00
(2.00-4.00) -1.00 0.681 0.539
DQI 75.37
(69.318-81.79) 78.74
(70.25-81.92) 3.37 0.519 6.68±2.26 6.52±1.80 -0.16 0.701 77.69
(69.71-82.18) 81.33
(78.30-83.66) 5.31 0.233 0.525
DQI-I 55.00
(45.00-60.00) 55.00
(45.00-63.75) 0.00 0.331 59.72±8.30 59.28±10.72 -0.44 0.835 57.33±9.23 61.33±11.56 4.00 0.344 0.312
Total oxidant
capacity
of diet
(mmol/100g)
7,72
(5,523-10,84) 7,76
(3,72-9,68) 0,04 0,204 7,73
(4,94-12,25) 7,76
(3,55-10,30) 0,03 0,137 7,28,55±3,39 7,26±3,52 -0,02 0,374 0,986
T0 : Baseline characteristics (before the intervention). T1 : Final characteristics (after the intervention). ∆: Delta, difference between final and initial period (∆ = T1 –T0). KCAL: Total calories of food frequency
questionnaire; w6/w3 ratio: omega 6/omega 3;RFS: Recommended food score; aMED score: Score Alternative Mediterranean Diet Score; HEI: Healthy Eating Index; DQI :Original Diet Quality index; DQI-I:
International Quality Diet Index.
Presented data: mean ± standard deviation or median (Q1-Q3) as parametria. Normality test: Kolmogorov- Smirnov, p < 0.05.
*a Paired Student t Test or Paired Wilcoxon Test . *b Student t Test or U-Mann- Whitney, for comparison between groups before the açaí intake
060_9135 El consumo de pulpa.indd 942 11/07/15 00:11
943
Nutr Hosp. 2015;32(2):931-945Açaí and inflammatory mediators
Furthermore, it was shown that overweight volun-
teers at baseline had a similar pattern food of eutro-
phic, despite differences in body composition. The
evaluation of the diet quality, by dietary indexes, be-
fore the acai consumption, showed that all volunteers
had a similar dietary pattern. In addition, the scores of
HEI, RFC, aMED, IDQ, DQI-I demonstrate the neces-
sity of improving the dietary patterns for both groups.
Followed by the stratification by group, after the acai
consumption, there was an increase only for the carbo-
hydrates consumption in the overweight group without
change the food pattern.
This interventional study about the beneficial effects
of acai in humans is the greatest executed so far. So, our
results provide interesting insights underlying the acai
intake consequence on the inflammatory status, food
intake, body composition and hormonal apparently
healthy women. Our work did not include a control of
acai intake, first because we understand that there is no
placebo for a fruit, consumed in a free-life context and
second because the volunteers were controls of them-
selves in the intervention, which allowed an intra-sub-
ject statistical analysis, enabling for the accuracy of the
results. As much as the monitoring of acai intake was
accomplished by means of food records before, during
and after the consumption, the intake of acai pulp, in a
free-living context, was not monitored, since the pro-
ject does not aimed to interfere in the food standard in
order to not induce any result.
In this cause-effect study, we cannot affirm that the
variables changes were due to a direct or indirect effect
of the acai pulp intake, it is important to emphasize that
the clinical experiment was carefully designed, espe-
cially for the precision in the duration of the interven-
tion and the amount of acai pulp offered to the volun-
teers. Thus, we consider this work relevant, since it will
provide the basis for further studies.
Conclusion
After the evaluation of inflammatory biomarkers,
food intake and body composition in eutrophic and
overweight women who consumed acai pulp du-
ring four weeks, it was observed an increase in the
pro-thrombotic marker PAI-1 and in the growth factor
EGF. These biomarkers are considered risk factors to
different diseases and are affected by oxidative stress
and inflammation, however, our study showed a pos-
sible modulation of them on anthropometric, bioche-
mical, inflammatory and dietary parameters by means
of the beneficial action of acai pulp intake. It impro-
ved the insulin sensitivity and reduced the PAI-1 on in
overweight women. In eutrophic group, it was obser-
ved a body fat redistribution, mainly to truncal region
with possible increase in intramuscular and visceral fat,
besides a subcutaneous body fat reduction. However in
the overweight group, there was a reduction in body
fat, and the blood pressure, consequently, decreased.
Our findings have shown that dietary pattern may
reflect the modulation of inflammation or a set of an-
thropometric, biochemical, clinical and inflammatory
changes inducing an imbalance of inflammatory me-
diators which act by inhibiting or promoting DC.
Competing interests
The authors declare they have no competing inte-
rests.
Author contributions
ISP: conducted field work, data collection, labora-
tory processing of samples, statistical analysis, wrote
and edited the manuscript; TCMCMP, RALV, GAFF:
conducted field work, data collection, laboratory pro-
cessing of samples and statistical analysis; FLPO: gui-
ded the statistical analysis and edited the manuscript;
FCS, JFA: guided the field work and laboratory pro-
cessing as well as edited the manuscript; RNF: project
co-lider, guided the field work and laboratory proces-
sing as well as edited the manuscript; ACPV: project
leader and general coordinator, performed the finan-
cial management, designed the study, guided the field
work and laboratory processing, besides edited the
manuscript. All authors read and approved the final
manuscript.
Acknowledgments
The authors are grateful to Lídia Mara Gomes Hen-
riques and Fernanda Campos Freire for helping in
collection and processing data, to all the voluntieers,
wich kindling participated of this study, and to Univer-
sidade Federal de Ouro Preto (UFOP), Coordenação de
Aperfeiçoamento do Ensino Superior do Ministério da
Educação do Brasil (CAPES), Conselho Nacional de
Pesquisa e Desenvolvimento Científico e Tecnológico
(CNPq) and Fundação de Amparo à Pesquisa do Estado
de Minas Gerais (FAPEMIG) for the financial support,
by means of following grants: CDS-APQ-04495-10
(Edital Programa Primeiros Projetos- 15/2010) e
475417/2013-5 (Edital Universal -14/2013), which
enable this work .
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