Nutr Hosp. 2016; 33(2):277-283  ISSN 0212-1611 - CODEN NUHOEQ  S.V.R.

318

Nutrición
Hospitalaria

Trabajo Original Obesidad y síndrome metabólico

Influence of the unsaturated fatty acids on body weight, glucose, and lipids
metabolism in obese women with Pro12Pro genotype in PPARγ2 gene
Influencia de los ácidos grasos insaturados en el peso corporal y en el metabolismo de la glucosa
y de los lípidos en mujeres obesas con el genotipo Pro12Pro en el gen PPARγ2
Márcia Fófano do Lago1, Vanessa Chaia Kaippert2, Débora Lopes Souto3 and Eliane Lopes Rosado4
Department of Nutrition and Dietetics and 2Nutrition Evaluation Laboratory. Federal University of Rio de Janeiro. Institute of Nutrition Josué de Castro. Rio de Janeiro, Brazil
1,3,4

Abstract
Background: The type of dietary fatty acid may have different effects on obesity and its complications, however, these effects can be influenced
by genes and polymorphisms, such as peroxisome proliferator-activated receptor γ isoform 2 (PPARγ2). Moreover, it is unclear whether the degree
of unsaturation of the fat has different effects on lipid and glucose metabolism, and particularly the loss of body weight.
Objective: To evaluate the influence of diets rich in polyunsaturated fatty acids (PUFA) and monounsaturated fatty acids (MUFA) on anthropometric
and biochemical variables in obese woman with genotype Pro12Pro on PPARγ2 gene on body weight, glycemic and lipemic profile.
Methods: Eighteen obese women with Pro12Pro genotype in PPARγ2 gene were randomized into groups to receive a high PUFAs (PUFA-diet,
n = 8) or MUFAs (MUFA-diet, n = 10) diets. Anthropometrics (body mass index [BMI] and waist circumference) and biochemical variables (glu-
cose, insulin, HOMA-IR, total cholesterol, LDL-cholesterol, and HDL-cholesterol and triglycerides) were evaluated at baseline and after 45 days.
Key words:
Results: Anthropometric and biochemical variables were similar between groups at baseline and after intervention (p > 0.05). BMI decrease only
Obesity. PPARγ2. in PUFA-diet (p = 0.01), probably due to the lower lipid content in this diet. MUFA-diet decrease fasting glucose (p = 0.03), insulin (p = 0.03),
Unsaturated fatty and HOMA-IR (p = 0.02).
acids. Body weight.
Insulin resistance. Conclusion: Compared to PUFA, MUFA was more efficient to reduce the insulin resistance in obese women with Pro12Pro genotype in PPARγ2,
Lipids metabolism. even in high saturated fatty acids and total fat diet.

Resumen
Introducción: el tipo de ácido graso de la dieta presenta diferentes efectos sobre la obesidad y sus complicaciones, pero estos efectos pueden
verse influenciados por los genes y sus polimorfismos, tales como los receptores activados por el proliferador de los peroxisomas isoforma γ2
(PPARγ2). Además, no está claro si el grado de insaturación de los lípidos posee diferentes efectos en el metabolismo de los lípidos y de la
glucosa y, particularmente, en la pérdida de peso.
Objetivos: evaluar la influencia de dietas ricas en ácidos grasos poliinsaturados (AGPI) y monoinsaturados (AGMI) en las variables antropométricas
y bioquímicas en el peso corporal y el perfil glucémico y lipémico en mujeres obesas con el genotipo Pro12Pro en el gen PPARγ2.
Métodos: dieciocho mujeres obesas con genotipo Pro12Pro fueron distribuidas aleatoriamente para una de las dietas, rica en AGPI (n = 8) o
Palabras clave: AGMI (n = 10). Las variables antropométricas (índice de masa corporal [IMC] y circunferencia de la cintura) y bioquímicas (glucosa, insulina,
Obesidad. PPARγ2. HOMA-IR, colesterol total, LDL-colesterol, HDL-colesterol y triglicéridos) fueron evaluadas antes y después de un periodo de 45 días.
Ácidos grasos Resultados: las variables antropométricas y bioquímicas fueron similares entre los grupos antes y después de la intervención (p > 0,05). El IMC
insaturados. Peso disminuyó después de la ingesta de AGPI (p = 0,01), probablemente debido al menor contenido de lípidos. El AGMI redujo la glucosa (p = 0,03),
corporal. Resistencia insulina (p = 0,03) y HOMA-IR (p = 0,02).
a la insulina.
Metabolismo de Conclusión: los AGMI fueron más eficientes para reducir la resistencia a la insulina en mujeres obesas con el genotipo Pro12Pro en el gen
lípidos. PPARγ2, aunque las mujeres presentaran una elevada ingesta de lípidos totales y ácidos grasos saturados.

Received: 15/09/2015 Correspondence:

Accepted: 02/11/2015
Débora Lopes Souto. Department of Nutrition and
Financial support: CNPq and FAPERJ. Dietetics. Federal University of Rio de Janeiro, Institute
of Nutrition Josué de Castro. 373 Carlos Chagas Filho
Lago MF, Kaippert VC, Souto DL, Rosado EL. Influence of the unsaturated fatty acids on body weight, Av. Health Sciences Center. Sector J, 2nd floor.
glucose, and lipids metabolism in obese women with Pro12Pro genotype in PPARγ2 gene. Nutr Hosp Ilha do Fundão. 21941-590 Rio de Janeiro. Brazil
2016;33:277-283 e-mail: [email protected]
278 M. L. Fófano et al.

INTRODUCTION cholesterol and HDL. Dietary intakes of PUFA n-3 fatty acids in-
duced changes in lipid metabolism by decreasing triacylglycerol
Obesity results from an imbalance between energy intake and concentrations, and may reduce the fraction of atherogenic small
energy expenditure, and may be defined as a disease in which and dense LDL, even in the absence of LDL lowering (5).
excess body fat has accumulated (1). Obesity increases the risk Dietary intakes of PUFA may also affect glucose metabolism. PUFA
of cardiovascular disease and has been strongly associated with n-6 fatty acids may modulate cytokine production or the release of the
dyslipidemia and insulin resistance (2). soluble tumor necrosis factor alpha receptors through eicosanoid-in-
Body weight is determined by an interaction between genetic, dependent pathways, affecting insulin signal transduction processes (5).
environmental and psychosocial factors acting through the physio- In the past, monounsaturated fatty acids (MUFA) were considered
logical regulation of energy intake and energy expenditure (2). to be neutral with regard to their influence on serum lipids and lipo-
Several candidate genes have been associated with human obesity. proteins. However, studies have suggested that MUFAs may also have
Among these genes, there is the peroxisome-proliferator-activated favorable effects on blood lipid concentrations. Two meta-analysis
receptor (PPAR) that is a member of the nuclear hormone receptor reported that a high MUFA-diet reduces fasting plasma triacylglycerol
superfamily. The predominant isoform of PPAR is the γ2 (PPARγ2), levels, as well as the susceptibility of LDL particles to oxidation; even no
which is expressed selectively and at higher level in adipose tissue, changes were noted in concentrations of HDL or LDL cholesterol (7,8).
where it modulates the expression of target genes implicated in adipo- Zheng et al. have suggested that MUFA intake activates synthetic and
cyte differentiation and glucose homeostasis. A point mutation found rapid catabolic pathways for triglyceride-rich lipoprotein metabolism
on the B exon of the NH2-terminal of PPARγ2, substituting alanine for that involve apolipoprotein E and apolipoprotein C-III, and suppresses
proline at position 12 (PPARγ Pro12Ala SNP) (rs1801282), has been the metabolism of more slowly metabolized VLDLs and doubles the
shown to decrease receptor activity (3). The Pro12Ala polymorph- direct clearance of triglyceride-rich lipoprotein from the circulation (9).
ism of the PPARγ2 isoform has an Ala12 allele frequency of around Studies have shown that the MUFA-diet increases insulin secre-
0.12 in Caucasians, and this variant may contribute to the observed tion (7,10). However, few studies have attempted to investigate the
variability in body mass index (BMI), and was associated with greater mechanisms by which dietary MUFAs mediate these benefits, and a
insulin sensitivity and a more favorable lipid profile (4). Therefore, hypothesis would explain this effect including the incretin hormone
genetic influences increase the risk of weight gain but they are not pathway. Paniagua et al. (10) and Rocca et al. (11) have found that
sufficient to explain the development of obesity. Other factors are MUFA increases secretion of glucagon-like peptide-1 (GLP-1). Ac-
implied in obesity such as lifestyle, dietary habits and environment (1). cording to López et al. (12), MUFA may modulate the postprandial
Different types of fatty acids display different metabolic behav- hyperactivity of beta-cells through GLP-1 and glucose-dependent in-
iors, such as oxidation and deposition rate differences, that may sulinotropic polypeptide (gastric inhibitory polypeptide [GIP]). GLP-1
contribute to body weight change (5). has an antidiabetic action through its ability to stimulate insulin se-
Polyunsaturated fatty acids (PUFAs) may be classified in n-3 fatty cretion, inhibit beta cell apoptosis, inhibit glucagon secretion, and
acids and n-6 fatty acids. The predominant n-6 fatty acid is arachi- delay gastric emptying and induce satiety. GIP also promotes energy
donic acid, which is converted to prostaglandins, leukotrienes and storage via direct actions on adipose tissue. Therefore, stimulating GIP
other lipoxygenase or cyclooxygenase products (important regulators and GLP-1 secretion results in a positive stimulation of beta-cells to
of cellular functions with inflammatory, atherogenic and prothrombotic increase insulin secretion (11).
effects). The n-3 fatty acids are docosahexaenoic acid (DHA) and MUFA may also be an agonist for PPAR, because MUFAs inhibit
eicosapentaenoic acid (EPA), which are competitive substrates for the acyl-CoA oxidase, which is involved in beta-oxidation, to indirectly
enzymes and products of arachidonic acid metabolism that antagon- increase accumulation of acyl-CoA leading to PPAR activation (13).
ize the pro-inflammatory effects of n-6 fatty acids (5). Since the precise mechanisms underlying the beneficial effects
Dietary linoleic acid (the long-chained n-6; 18:2) is converted to of these fatty acids are not yet fully understood, and they are nat-
arachidonic acid, which serves as a precursor for prostaglandins. ural PPAR ligands, we investigated the influence of unsaturated
A metabolite of these prostaglandins (5-deoxy-D12, 14-prosta- fatty acids intake on anthropometric and biochemical variables in
glandin J2) was shown to stimulate the differentiation of preadi- obese woman, carriers of the wild-type homozygous genotype
pocytes into adipocytes through its interaction with the PPARγ2. in the PPARγ gene (Pro12Pro).
Another prostaglandin (prostaglandin F2α) blocks adipogenesis
through activation of the mitogen-activated protein kinase, re-
sulting in inhibition of adipocyte gene expression PPARγ2 (6). METHODS
The beneficial properties of n-3 PUFAs have been observed in
populations consuming large amounts of cold-water fish (e.g., CASUISTRY
salmon and tuna), vegetable oils (e.g., soybean and canola), nuts
(e.g., walnuts), and seeds (e.g., flaxseed). Foods that contain n-6 This study was conducted in the Institute of Nutrition Josué de
PUFAs include other vegetable oils (e.g., corn and sunflower, and Castro at the Federal University of Rio de Janeiro (Brazil).
sesame), cereal grains, meat, milk, and eggs (5). Volunteers were recruited through poster advertisements at the
The dietary linoleic acid (ALA, a dietary n-6 polyunsaturated Clementino Fraga Filho University Hospital, Brazil (between March
fatty acid) may be associated with a reduction of the ratio total 2006 and October 2007).

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INFLUENCE OF THE UNSATURATED FATTY ACIDS ON BODY WEIGHT, GLUCOSE, AND LIPIDS METABOLISM IN OBESE 279
WOMEN WITH Pro12Pro GENOTYPE IN PPARγ2 GENE

Table I. Anthropometric and biochemical variables at baseline and after intervention in

PUFA-diet and MUFA-diet in each group
PUFA-diet MUFA-diet
p-value‡ p-value§
Levels* Δ* p-value †
Levels* Δ* p-value†
BMI (kg/m2) 44.17 ± 2.94 44.61 ± 3.70
0.80
Baseline (41.00 – 47.80) -1.08 ± 0.57 (39.80 – 50.70) -0.96 ± 0.55
0.01 0.05 0.62
BMI (kg/m2) 43.08 ± 3.02 (-2.00 – -0.30) 43.64 ± 3.88 (-1.70 – -0.10)
0.84
After intervention (39.70 – 47.20) (38.10 – 49.34)
Waist circumference (cm) 122.80 ± 7.99 125.77 ± 10.38
0.42
Baseline (114.50 – 140.00) -3.57 ± 2.33 (107.00 – 140.00) -2.95 ± 3.02
0.01 0.01 0.44
Waist circumference (cm) 119.22 ± 8.19 (-8.00 – -1.00) 122.82 ± 11.34 (-8.70 – 0.00)
0.37
After intervention (110.00 – 135.00) (104.50 – 139.00)
Waist-hip ratio 0.29 ± 0.06 0.86 ± 0.08
1.00
Baseline (0.18 – 0.34) 0.56 ± 0.13 (0.73 – 0.98) -0.60 ± 0.08
0.01 < 0.01 0.47
Waist-hip ratio 0.86 ± 0.08 (0.39 – 0.75) 0.30 ± 0.06 (44.00 – 74.00)
0.32
After intervention (0.73 – 0.98) (0.23 – 0.41)
Glucose (mg/dl) 86.00 ± 9.35 103.88 ± 27.28
0.28
Baseline (71.00 – 102.00) 0.37 ± 8.63 (71.00 – 122.00) -12.33 ± 15.75
0.73 0.03 0.09
Glucose (mg/dl) 86.37 ± 7.34 (-15.00 – 12.00) 91.55 ± 19.00 (-42.00 – 9.00)
0.88
After intervention (76.00 – 98.00) (0.18 – 0.34)
Insulin (mUI/l) 9.32 ± 4.84 15.87 ± 7.77
0.22
Baseline (4.80 – 19.40) -1.71 ± 5.94 (4.90 – 26.6) -7.92 ± 8.37
0.48 0.03 0.11
Insulin (mUI/l) 9.32 ± 4.84 (-12.70 – 6.20) 7.95 ± 2.16 (-18.40 – 3.66)
0.96
After intervention (4.80 – 19.40) (3.60 – 10.70)
HOMA-IR 2.35 ± 0.88 4.20 ± 2.45
0.17
Baseline (1.16 – 3.76) -0.37 ± 1.21 (0.98 – 4.17) -2.44 ± 2.40
0.57 0.02 0.05
HOMA-IR 1.98 ± 1.03 (-2.78 – 0.84) 1.76 ± 0.54 (-6.08 – 0.74)
0.92
After intervention (0.98 – 4.17) (1.00 – 2.77)
Total cholesterol (mg/dl) 196.25 ± 27.52 192.30 ± 42.34
0.85
Baseline (152.00 – 224.00) -16.76 ± 43.80 (133.00 – 212.00) -7.60 ± 46.00
0.40 0.87 0.56
Total cholesterol (mg/dl) 179.50 ± 26.95 (-91.00 – 58.00) 184.70 ± 52.71 (-117.00 – 35.00)
0.82
After intervention (133.00 – 212.00) (83.00 – 275.00)
HDL-cholesterol (mg/dl) 45.37 ± 13.20 42.30 ± 9.75
0.59
Baseline (31.00 – 75.00) 0.75 ± 14.52 (22.00 – 55.00) 3.40 ± 9.16
0.67 0.26 0.24
HDL-cholesterol (mg/dl) 44.62 ± 6.90 (-14.00 – 28.00) 45.70 ± 8.42 (-10.00 – 21.00)
0.39
After intervention (32.00 – 57.00) (32.00 – 59.00)
LDL-cholesterol (mg/dl) 127.25 ± 23.91 127.10 ± 36.10
0.72
Baseline (93.00 – 164.00) -12.37 ± 16.76 (81.00 – 191.00) -5.30 ± 26.96
0.09 0.61 0.30
LDL-cholesterol (mg/dl) 114.87 ± 23.29 (-34.00 – 15.00) 127.25 ± 23.91 (-63.00 – 25.00)
0.79
After intervention (80.00 – 153.00) (93.00 – 164.00)
Triglycerides (mg/dl) 101.12 ± 74.32 115.10 ± 63.17
0.13
Baseline (52.00 – 277.00) -6.75 ± 57.06 (45.00 – 277.00) -8.10 ± 69.89
0.32 0.87 0.85
Triglycerides (mg/dl) 94.37 ± 30.52 (-143.00 – 39.00) 107.00 ± 48.43 (-160 – 76.00)
0.59
After intervention (58.00 – 137.00) (38.00 – 203.00)
*
Means ± standard deviations (95% CI). Delta (Δ): Measured as the difference between after intervention and baseline values after intervention period. †p-values were
derived by analysis of covariance with basal and after intervention values after each group (Wilcoxon signed rank test). ‡p-values were derived by Mann-Whitney test
to compare basal and after intervention values between the groups. §p-values were derived by Mann-Whitney test to compare the difference of delta (Δ) between after
intervention and baseline values between the groups.

[Nutr Hosp 2016;33(2):277-283]

280 M. L. Fófano et al.

The sample size and the selection of women were for conven- Diagnostica S.A., Brazil; HDL Cholesterol, Labtest Diagnostica
ience (14). All participants signed an informed consent, and the S.A., Brazil; and triglycerides Liquiform, Labtest Diagnostica S.A.,
study was approved by the Ethical Committee (Institutional Review Brazil).
Board, protocol 116/05). LDL-cholesterol concentrations were determined using the
The inclusion criteria considered were: adult women with a Friedewald equation (18).
family history of obesity, lack of menopause, and BMI greater The determination of plasma glucose was performed using the
than 35 kg/m2 (15). commercial kit GLUCOSE PAP Liquiform (Labtest Diagnostica S.A.,
Exclusion criteria were smoking, alcoholism, cardiovascular Brazil).
diseases, chronic kidney disease, diabetes mellitus and/or other Serum insulin was analyzed using the commercial kit
chronic diseases, infectious diseases, pregnancy, use of antibiotics COAT-A-Count® (Diagnostic Products Corporation®, USA).
or anti-inflammatory drugs, antidiabetic medications, lipid-lowering Hyperinsulinemia was considered in volunteers with fasting
drugs, diuretics, antidepressants, antihypertensive, and drugs sup- insulin > 9 μU/Ml(19).
plements and/or herbal remedies for weight loss, dieting for weight Insulin resistance (IR) was estimated by calculating homeosta-
loss in the last four weeks, or weight loss greater than 3 kg in the sis model assessment (HOMA-IR). IR values were considered as
last month. HOMA-IR ≥ 2.71 (20).

STUDY DESIGN ANTHROPOMETRY ASSESSMENT

This is a controlled randomized clinical-trial. All volunteers were BMI was calculated as body weight in kilograms divided by the
assessed at baseline and after forty-five days of intervention. square of height in meters (15).
The participant arrived at the Laboratory of Clinical Analysis of Waist circumference (WC) was determined by the average of
the Pharmacy College at 7 h a.m. after twelve hours overnight fast. two measurements obtained at the midpoint between the lower rib
Upon arrival, venous blood glucose samples were collected and margin and the iliac crest after a normal expiration (21).
the anthropometric assessment was performed immediately after. Hip circumference was determined around the widest portion
Participants were allocated into two groups to receive a diet rich of the hip, and the waist-hip ratio was calculated as well (21).
in PUFA (PUFA-diet) or a diet rich in MUFA (MUFA-diet).
Fortnightly, they received individual face-to-face consultation
sessions which included advices on food purchase and selection, GENOTYPING PPARγ2
portion sizes, and cooking methods. In these consultations, an-
thropometry was assessed and 24-hour recalls were performed Molecular analyses were performed in the Laboratory of
to verify adherence to the diet. Molecular Biology of Cancer, at the Federal University of Rio
de Janeiro.
Genomic DNA was extracted from samples of whole blood using
DIETETIC INTERVENTION a commercial kit (MasterPureTM Genomic DNA Purification Kit,
Epicentre®, Biotechnologies) and stored at -20 °C until the sub-
All participants received an individualized diet based on the sequent step.
total energy expenditure (estimated according to FAO/WHO [16]) Determination of the Pro12Pro genotype was performed using
with an energy deficit of 500-1.000 kcal/day achieved through the polymerase chain reaction-restriction fragment-length poly-
reductions in total energy intake (17). morphism (PCR-RFLP) method, according to the sequences avail-
Energy from macronutrients was similar in both groups (dietary able in the Gen Bank DNA AB005520, and according previous
energy content of 50-60% carbohydrates, 15-20% of protein, described for us (22).
30% of total fat), and both diets have less than 10% of saturated The sequences of PCR primers were: 5’-GCC AAT TCA AGC
fatty acids (SFA), based on current recommendations (16). CCA GTC-3 ‘and 5’-GCC ATG TTT GCA GAC AGT GTA TCA GTG
The PUFA-diet consisted of 15% of PUFA and 10% of MUFA, and AAG GAA TCG CTT TCC G- 3’. The cycling conditions were as
the MUFA-diet consisted of 10% of PUFA and 15% of MUFA. follows: an initial denaturation at 95 °C for 5 minutes, followed
The analysis of the chemical composition of the diets was con- by 35 cycles of denaturing at 95 °C for 30 seconds, annealing
ducted in Food Processor program version 12 (Esha Research, at 59 °C for 30 seconds and extension at 72 °C for 30 seconds.
Salem, USA, 1984). The final extension was continued at 72 °C for 10 minutes
and cooling to 4°C. The generated fragment was 267 bp (base
pairs).
BIOCHEMICAL MEASUREMENTS After enzymatic digestion of the PCR products (60 °C for
180 minutes) by Bst UI restriction endonuclease (New England
Total cholesterol, HDL-cholesterol and triglycerides were meas- Biolabs, Inc.), fragments of 267 bp were generated, indicating the
ured using the commercial kits (Cholesterol Liquiform, Labtest presence of wild type homozygous genotype (Pro12Pro).

[Nutr Hosp 2016;33(2):277-283]

INFLUENCE OF THE UNSATURATED FATTY ACIDS ON BODY WEIGHT, GLUCOSE, AND LIPIDS METABOLISM IN OBESE 281
WOMEN WITH Pro12Pro GENOTYPE IN PPARγ2 GENE

DIETARY INTAKE ASSESSMENT both groups (PUFA-diet: -3.57 ± 2.33 cm; MUFA-diet: -2.95 ± 3.02 cm)
(p = 0.01). BMI decreased only in PUFA-diet (-1.08 ± 0.57 kg/m2;
Volunteers filled in a 3-day food record (2 weekdays and 1 week- p = 0.01), and only MUFA-diet decreased fasting glucose (-12.33 ±
end day). During those three days, all foods and drinks consumed 15.75 mg/dl; p = 0.03), insulin (-7.92 ± 8.37 mUI/l; p = 0.03) and
had to be documented to allow quantitative estimation of dietary HOMA-IR (-2.44 ± 2.40; p = 0.02).
intake. The 3-day energy and nutrient intakes were averaged to However, the variation (delta) after intervention and baseline values
obtain a mean daily energy and nutrient intake for each volunteer. between groups showed that the anthropometric and biochemical
Volunteers were followed fortnightly when 24-hour recalls were variables did not differ between PUFA and MUFA-diets (p > 0.05).
performed to verify adherence to the diet. As shown in table II, there was no significant difference between
The individual food records of each volunteer were carefully groups for energy intake (p > 0.05) as calculated from 3-day food
checked, and data were then entered into the nutritional software records. However, total fat was higher in MUFA-diet compared to
(Food Processor software version 12, Esha Research, Salem, USA, PUFA-diet (p < 0.01). As we wanted, PUFA intake was higher in
1984), after the adjustment for the typical Brazilian diet. the PUFA-diet group (p = 0.02), while the group with MUFA-diet
presented a higher MUFA intake (p = 0.02). Both groups intake
more than 10% of SFA, however, there was no difference be-
STATISTICAL ANALYSIS tween groups. The other nutrients did not differ between groups
(p > 0.05).
Statistical analyses were performed in SPSS software (ver- PUFA intake was not associated with any of the anthropometric
sion 17.0; SPSS Inc, Chicago, IL) with 5% significance level. or laboratory variables (p > 0.05). However, MUFA intake showed
To check the distribution of continuous variables (clinical, an- a negative association with the HOMA-IR (r = -0.52; p = 0.03) in
thropometric and biochemical) the test of Kolmogorov-Smirnov both groups, and regression analysis showed an association be-
was performed (1: age; 2: body weight, BMI and WC; 3: serum tween the HOMA-IR and MUFA intake only in MUFA-diet (r = 0.71;
insulin, plasma glucose, triglycerides, total cholesterol and frac- p = 0.02).
tions [HDL, LDL and VLDL] and values of HOMA-IR and QUICK).
For the comparison between the means of the groups, the basic
statistics of location (mean) and dispersion (standard deviation) DISCUSSION
were calculated.
Continuous variables presented normal distribution and the In the present study, no differences were found in anthropomet-
parametric Student t test for the comparison between groups was ric and biochemical variables comparing PUFA- and MUFA-diets.
used. When the variance was less than 4, we used the Student t However, the intragroup evaluation has shown that BMI decreased
test for equal variances; otherwise, we applied the Student t test only in PUFA-diet, and fasting glucose, insulin and HOMA-IR
for different variances. decreased only in MUFA-diet. The methodological care in this
study is an advantage, since other studies evaluating the effect
of unsaturated fats in weight loss and lipid and glucose profile do
RESULTS not standardize the studied population considering the presence
of genetic variants, particularly of nuclear transcription factors.
Among women recruited, only one had the genotype variant We only recruit women carriers of the homozygous genotype
(Ala12Ala), and she was therefore excluded from the study. All (Pro12Pro) because the presence of genetic variant may alter the
others eighteen volunteers presenting the genotype Pro12Ala lipidic and glicidic metabolism (23).
were included in the study. Studies have supported the fact that MUFAs and PUFAs may
Ten volunteers (55.5%) used the MUFA-diet while eight (44.4%) act as ligands of PPARγ2, increasing GLUT4 transcription and
used the PUFA-diet. improving insulin resistance (24,25). Our results demonstrated
The characteristics of each group are presented in table I. They that MUFA intake is more effective than PUFA intake to improve
presented a mean age of 36.7 ± 6.08 (IC: 23-46), and a mean BMI HOMA-IR values.
of 44 ± 3.31 kg/m2 (IC: 39.8-50.70). Anthropometric and biochemical Studies have shown that MUFA intake may increase the re-
characteristics were similar between groups at baseline (p > 0.05). sponse of pancreatic beta-cells to improve insulin sensitivity,
increase incretins production (like GLP-1) and reduce insulin
clearance (10,11). Thus, guidelines affirm that high MUFA-diet
CHARACTERISTICS OF GROUPS AFTER improves HOMA-IR in insulin-resistant subjects (26).
INTERVENTION Previous studies identified no difference in insulin sensitivity
between diets rich in SFA versus MUFA or PUFA versus MUFA, or
The characteristics of groups after intervention are also pre- all three (27,28). However, other studies have showed conclusions
sented in table I. similar to our results (29,30). Thus, based on these data, we
Waist-hip ratio increased in PUFA-diet (0.56 ± 0.13; p = 0.01) and suggest a preference for MUFA over PUFA for improved insulin
decreased in MUFA-diet (-0.60 ± 0.08; p < 0.01), and WC decreased in sensitivity.

[Nutr Hosp 2016;33(2):277-283]

282 M. L. Fófano et al.

Table II. Energy and fat intake during the intervention in PUFA-diet and MUFA-diet
PUFA-diet (n = 8) MUFA-diet (n = 10) p value‡
Energy (kcal) 1,993.02 ± 692.91 2,378.51 ± 812.42 0.18
Fat intake (%) 31.66 ± 4.48 39.10 ± 5.54 < 0.01
Saturated fatty acids intake (%) 11.40 ± 3.41 14.49 ± 2.91 0.06
Polyunsaturated fatty acids intake (%) 5.98 ± 1.34 6.33 ± 1.33 0.02
Monounsaturated fatty acids intake (%) 11.35 ± 2.33 14.92 ± 3.21 0.02
Data are mean ± SD; p-values were derived by Mann-Whitney test.
‡

Our results showed that PUFA-diet increased and MUFA-diet CONCLUSIONS

reduced the waist-hip ratio, and both unsaturated fatty acids
have reduced the waist circumference. Therefore, improvement To conclude, current data show that MUFA-diet is more efficient
in insulin sensitivity was not associated with reduction of waist than PUFA-diet to reduce the insulin resistance in obese women
circumference, but with the possible favorable effect of the with Pro12Pro genotype in PPARγ2, despite the high total fat and
MUFA-diet on endothelial function. SFA content in MUFA-diet.
Previous studies demonstrated that a high dietary SFA or n-6
fatty acids (PUFA) are significant independent predictors of fasting
hyperinsulinemia (27,28). In contrast, the favorable effect of the ACKNOWLEDGEMENTS
MUFA-diet on endothelial function might be attributed to the in-
hibition of the expression of leukocyte adhesion molecules (7-9). We would like to thank volunteers who participated in the study,
Therefore, we suggest that the specific dietary fat may influence Sofia Kimi Uehara (Ph. D. Nutrition Sciences at Federal University
body fat distribution and insulin sensibility without affecting of Rio de Janeiro), Dr. Franklin D. Rumjanek, Nivea Amoedo and
total body weight. other employees of the Laboratory of Molecular Biology of Cancer,
In addition, we found a BMI reduction in response to caloric at the Federal University of Rio de Janeiro; Dr. Maria de Fátima
restriction, independently of unsaturated fatty acids diets. This is Santos de Oliveira and other professionals from the Association of
consistent with Garaulet et al. study, which reported a lesser re- Parents and Friends of Exceptional Children-Tijuca, Rio de Janeiro;
sistance to weight loss in individuals with the Pro12 carriers (31). and Dr. Marcos Fleury, from the Laboratory of Clinical Analyses of
Even though no significant differences between groups were the Pharmacy College of the Federal University of Rio de Janeiro,
found, we observed that the PUFA-diet led to a greater decrease of and other laboratory employees.
body weight compared with MUFA-diet. We know that PUFA serves
as a precursor for prostaglandins, which play a critical role in β-oxi-
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INFLUENCE OF THE UNSATURATED FATTY ACIDS ON BODY WEIGHT, GLUCOSE, AND LIPIDS METABOLISM IN OBESE 283
WOMEN WITH Pro12Pro GENOTYPE IN PPARγ2 GENE

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