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The increase in lean mass is directly related to the loss of independence, muscle strength, and worse quality of life over the years. Studies in epigenetics can provide accurate answers about lean mass, demonstrating changes in DNA methylation patterns and possible changes in gene expression. The objective of this study was to verify whether there is a difference in the methylation profile among Brazilian women aged 50 to 70 years with greater or lesser lean mass. A cross-sectional study comprised 22 women aged 50 to 70 years, with 2 groups of 11 participants (Low Lean Mass and More Lean Mass). Lean mass was measured by dualenergy X-ray emission densitometry (DEXA). Blood DNA was collected for methylation assays using the Illumina 850k EPIC Infinium Methylation BeadChip, analyzing data from the Bioconductor chAMP data package medium in RStudio software. We obtained 1,913 differentially methylated (p ≤ 0.005 of delta β > 5% and delta β < −5 %) with a total of 979 genes with different methylation sites between groups (p ≤ 0.005; −5% > delta β > 5%). In addition, the pathway with the greatest power of significance was PI3K-Akt, presenting an FDR of 4.6 x 10-3. Thus, our results demonstrate a differentiation between specific sites of different genes, which have essential functions in body composition and energy metabolism, supporting future studies that aim to relate lean mass with epigenetics.

BACKGROUND/OBJECTIVES Genes involved in the regulation of metabolism, adipose tissue deposition, inflammation, and the appetite-satiety axis may play an important role in fetal development, and possibly induce permanent metabolic changes and fat accumulation. In this study we investigated: (1) obesity-related gene expression in maternal and cord blood of overweight/obese and normal-weight pregnant women; (2) associations between obesity-related gene expression in maternal and cord blood; and (3) associations of gene expression in each of maternal and cord blood with newborn adiposity. SUBJECTS/METHODS Twenty-five overweight/obese and 32 normal-weight pregnant women were selected from the Araraquara Cohort Study according to their pre-pregnancy BMI. Maternal and cord blood gene expression of LEPR, STAT3, PPARG, TLR4, IL-6, IL-10, FTO, MC4R, TNF-α, and NFκB were investigated by relative real-time PCR quantification. The body composition of the newborns was assessed by air displacement plethysmography. Associations between maternal and cord blood gene expression and markers of newborn adiposity (weight, BMI, and fat mass%) were explored by linear regression models controlling for maternal age, pre-pregnancy BMI, maternal gestational weight gain, gestational age, and newborn sex. RESULTS There was higher TLR4, NFκB, and TNF-a expression, and lower IL-6 expression, in overweight/obese pregnant women and their respective newborns compared with normal-weight women and their newborns (p

Obesity is directly connected to lifestyle and has been associated with DNA methylation changes that may cause alterations in the adipogenesis and lipid storage processes contributing to the development of the disease. We demonstrate a complete protocol from selection to epigenetic data analysis of patients with and without obesity. All steps from the protocol were tested and validated in a pilot study. 32 women participated in the study, in which 15 individuals were classified with obesity according to Body Mass Index (BMI) (45.1 ± 5.4 kg/m

Telomeres are structures located at the ends of chromosomes associated with a protein complex, known as the shelterin complex. In individuals with obesity, excess adipose tissue plays a key role in inducing a chronic and systemic inflammatory state, which can cause TL shortening. In this context, bariatric surgery is one of the most effective treatment modalities in improving metabolic control. Therefore, the present study aimed to evaluate how a short postoperative period of gastric bypass affects TL and expression of POT1, TRF1 and TRF2 genes. Forty-eight women submitted to RYGB were evaluated before and after 6 months of the surgical procedure. Anthropometric measures of body weight and height (BMI), abdominal circumference (AC), body composition, food intake and blood collection for biochemical evaluation, TL analysis (DNA), and gene expression (RNA) were collected at each moment. There was a reduction of weight, BMI, AC, FM and FFM as well as of glycemia, total cholesterol, LDL-cholesterol, and triglycerides after gastric bypass. No difference in energy intake and macronutrients consumption was observed. There was no significant change in TL, but there was a significant increase of POT1 and TRF1 gene expression after surgery, while TRF2 expression did not change. Despite bariatric surgery is not capable of increasing telomere length in a short-term period, no reduction is observed; additionally, we found a correlation between serum triglycerides concentration and TL. The increase of POT1 and TRF1 gene expression may explain the maintenance of the TL after 6 months postoperative period.

We aimed to investigate the effects of short-term hypocaloric diet-induced weight loss on DNA methylation profile in leukocytes from women with severe obesity. Eleven women with morbid obesity (age: 36.9 ± 10.3 years; BMI: 58.5 ± 10.5 kg/m2) were assessed before and after 6 weeks of a hypocaloric dietary intervention. The participants were compared with women of average weight and the same age (age: 36.9 ± 11.8 years; BMI: 22.5 ± 1.6 kg/m2). Genome-wide DNA methylation analysis was performed in DNA extracted from peripheral blood leukocytes using the Infinium Human Methylation 450 BeadChip assay. Changes (Δβ) in the methylation level of each CpGs were calculated. A threshold with a minimum value of 10%, p

Telomeres are structures located at the ends of chromosomes associated with proteins, from the shelterin complex, which are responsible for the protection and preservation of the genetic material. The telomere length (TL) progressively decreases with each cell division, and recent evidence suggests that lifestyle can lead to telomere shortening. In individuals with obesity, excess adipose tissue plays a key role in inducing a chronic and systemic inflammatory state, which can cause TL shortening. Thus, the aim of the present review was to show the relationship between obesity and TL in addition to the possible risk factors for its shortening and how the different strategies for weight loss can modulate TL. As the crucial result, we can consider the association between TL and weight loss, and adiposity changes after different interventions, showing that TL may be used as a biomarker of responses to obesity treatment.

Aim: To analyze the association and susceptibility of Single Nucleotide Polymorphisms (SNPs) in the DRD2 and BDNF genes with BED in patients with weight regain in the postoperative period of bariatric surgery. Methods: 177 individuals who underwent bariatric surgery with weight regain were evaluated and divided into two groups according to the BED diagnostic. The individuals were submitted to an anthropometric evaluation, analysis of the presence of BED using a validated questionnaire, and blood collection for genotyping of the polymorphisms rs6265 (BDNF) and rs1800497 (DRD2) by Real-Time Polymerase Chain Reaction (RT-PCR). Results: the presence of wild-type alleles for rs1800497 (CC) and rs6265 (GG) were more frequent in patients without BED. Nevertheless, the presence of one or two variant alleles for rs1800497 (CT+TT) and rs6265 (GA+AA) was more frequent in patients with BED. The combination of the two studied SNPs prevailed in patients with BED. Conclusions: In the presence of polymorphisms rs1800497 in the DRD2 gene and rs6265 in the BDNF gene, isolated and/or combined could occur an additional risk for the development of BED in patients with obesity, especially in the context of weight regain.Level of evidence: III (evidence obtained from the case-control analytic study).

Background: Telomere length (TL) shortening process is associated with several known environment and individual determinants. DNA methylation is the most studied epigenetic process and may be associated with TL. We investigated the associations between DNA methylation and TL in peripheral blood. Methods: Methylation wide association study was conducted in 47 women (37.1±8.8 years) with different nutritional status. Association between TL and DNA methylation levels were explored by univariate and multiple linear regression models, corrected by age and Body Mass Index. Corrections for multiple comparisons by Benjamini‐Hochberg test was also performed. WEBGestalt was used to identify pathways that are responsible for regulating TL. Results: We found negative correlations between TL and BMI (r = -0.641; p = 0.001), abdominal circumference (r = -0.622; p = 0.001) and fat mass (r = -0.656; p = 0.001). 44 CpGs sites were associated with TL, independent of age and BMI. The most of these sites were negatively correlated with TL. For the 7 remained sites, DNA hypomethylation were associated with shorter TL. These CpGs were related to nine different pathways, including thermogenesis, cancer, glutamatergic and serotonergic synapse. Conclusion: There is an epigenetic contribution in TL, independent of nutritional status and age. Genes related to TL are involved in important metabolic pathways.

Summary Background & aims Obesity is associated with low grade systemic inflammation and insulin resistance. Although metabolic and immunological changes may contribute to the increased risk for COVID-19 mortality in obese, little is known about the impact of obesity in the lungs of patients with COVID-19. Methods We analyzed gene expression profiles of autopsy lungs of a cohort of 14 COVID-19 patients and 4 control individuals. Patients were divided into 3 groups according to their comorbidities: hypertension, type 2 diabetes (T2D) and obesity. We then identified the molecular alterations associated with these comorbidities in COVID-19 patients. Results Patients with only hypertension showed higher levels of inflammatory genes and B-cell related genes when compared to those with T2D and obesity. However, the levels of IFN-gamma, IL22, and CD274 (a ligand that binds to receptor PD1) were higher in COVID-19 patients with T2D and obesity. Several metabolic- and immune-associated genes such as G6PD, LCK and IL10 were significantly induced in the lungs of the obese group. Conclusion Our findings suggest that SARS-CoV-2 infection in the lungs may exacerbate the immune response and chronic condition in obese COVID-19 patients.

Summary Background & aims The worldwide outbreak of the coronavirus disease 2019 (COVID-19) has already caused a substantial public health burden. Increasing number of studies linked obesity to more severe COVID-19 consequence and mortality, challenging health systems worldwide, especially in emerging countries like Brazil. Herein, we aimed to search the literature and present the current intersection between obesity and COVID-19 in the Brazilian population. Methods One hundred twenty-five articles were initially searched after duplicate removal, and nine were finally included in our analysis. Results Our findings emphasized the magnitude of COVID-19 infection in Brazil and the impact of obesity as a risk factor that aggravates the prognosis of outpatients or hospitalized patients. We also demonstrated social aspects of COVID-19 that could act enhancing the obesity condition in Latin American countries. Conclusions A more careful look at the available data could help to understand better the dynamic between obesity and COVID-19, focusing on the Brazilian population and could eventually guide management strategies and therapies for COVID-19 in the future.

Beta-alanine has become a dietary supplement widely used by athletes due to its ergogenic effect. However, there is still no consensus on the performance benefit of beta-alanine on exercise lasting longer than ten minutes. The present study aimed to evaluate the effect of beta-alanine supplementation on running performance and the expression of TauT and PAT1.This double-blind, randomized study enrolled 16 long-distance runners (37±8 years) who were randomly allocated to two groups: placebo (PLA) and beta-alanine (BA) (4.8 g/day 1) for four weeks. Maximal oxygen consumption, anthropometry, body composition, and food intake were determined. Before and after the intervention, the athletes undertook a 5000 m running time trial. Venous blood (TauT and PAT1 expressions) and ear lobe capillary blood (lactate) collected before and after exercise. Between tests, we monitored the training variables.The results were analyzed by t-tests and an ANOVA of repeated measures, with Sidak's post hoc (P0.05). PLA exhibited lower body fat than BA (8.7±2.2 vs. 11.5±2.8%, P=0.04). After supplementation, there was an increase in PAT1 expression in BA when compared to PLA (1.17±0.47 vs. 0.77±0.18, P=0.04). No significant differences were shown for the 5000 m running time in PLA (PRE: 1128±72; POST: 1123±72s) and BA (PRE: 1107±95; POST: 1093±86s).Although beta-alanine supplementation increased PAT1 expression, there was no statistically significant improvement in 5000 m running performance. However, individual responses should be considered as the BA showed a higher delta than the PLA.

Background Telomere length is inversely associated with the senescence and aging process. Parallelly, obesity can promote telomere shortening. Evidence suggests that physical activity may promote telomere elongation. Objective This study’s objective is to evaluate the effects of combined exercise training on telomere length in obese women. Design and Methods Twenty pre-menopausal women (BMI 30–40 kg/m2, 20–40 years) submitted to combined training (strength and aerobic exercises), but only 13 finished the protocol. Each exercise session lasted 55 min/day, three times a week, throughout 8 weeks. Anthropometric data, body composition, physical performance (Vo2max), and 8-h fasting blood samples were taken before and after 8 weeks of training. Leukocyte DNA was extracted for telomere length by RT-qPCR reaction, using the 2−ΔΔCt methodology. Results After the training intervention, significant differences (p < 0.05) were observed in telomere length (respectively before and after, 1.03 ± 0.04 to 1.07 ± 0.04 T/S ratio), fat-free mass (46 ± 7 to 48 ± 5 kg), Vo2max (35 ± 3 to 38 ± 3 ml/kg/min), and waist circumference (96 ± 8 to 90 ± 6 cm). In addition, an inverse correlation between waist circumference and telomere length was found, before (r = − 0.536, p = 0.017) and after (r = − 0.655, p = 0.015) exercise training. Conclusion Combined exercise promoted leukocyte telomere elongation in obese women. Besides, the data suggested that greater waist circumference may predict shorter telomere length. Clinical Trial Registration ClinicalTrails.gov, NCT03119350. Retrospectively registered on 18 April 2017

[Abstract] DNA methylation could provide a link between environmental, genetic factors and weight control and can modify gene expression pattern. This study aimed to identify genes, which are differentially expressed and methylated depending on adiposity state by evaluating normal weight women and obese women before and after bariatric surgery (BS). We enrolled 24 normal weight (BMI: 22.5 ± 1.6 kg/m2) and 24 obese women (BMI: 43.3 ± 5.7 kg/m2) submitted to BS. Genome-wide methylation analysis was conducted using Infinium Human Methylation 450 BeadChip (threshold for significant CpG sites based on delta methylation level with a minimum value of 5%, a false discovery rate correction (FDR) of q

Differential gene expression in peripheral blood mononuclear cells (PBMCs) after Roux-en-Y gastric bypass (RYGB) is poorly characterized. Markers of these processes may provide a deeper understanding of the mechanisms that underlie these events. The main goal of this study was to identify changes in PBMC gene expression in women with obesity before and 6 months after RYGB-induced weight loss. The ribonucleic acid (RNA) of PBMCs from 13 obese women was analyzed before and 6 months after RYGB; the RNA of PBMCs from nine healthy women served as control. The gene expression levels were determined by microarray analysis. Significant differences in gene expression were validated by real-time quantitative polymerase chain reaction (RT-qPCR). Microarray analysis for comparison of the pre- and postoperative periods showed that 1366 genes were differentially expressed genes (DEGs). The main pathways were related to gene transcription; lipid, energy, and glycide metabolism; inflammatory and immunological response; cell differentiation; oxidative stress regulation; response to endogenous and exogenous stimuli; substrate oxidation; mTOR signaling pathway; interferon signaling; mitogen-activated protein kinases (MAPK), cAMP response element binding protein (CREB1), heat shock factor 1 (HSF1), and sterol regulatory element binding protein 1c (SREBP-1c) gene expression; adipocyte differentiation; and methylation. Six months after bariatric surgery and significant weight loss, many molecular pathways involved in obesity and metabolic diseases change. These findings are an important tool to identify potential targets for therapeutic intervention and clinical practice of nutritional genomics in obesity.

Although energy restriction contributes to weight loss, it may also reduce energy expenditure, limiting the success of weight loss in the long term. Studies have described how genetics contributes to the development of obesity, and uncoupling proteins 1 and 2 (UCP1 and UCP2) and beta-3-adrenoceptor (ADRB3) have been implicated in the metabolic pathways that culminate in this condition. This study aimed to evaluate how the UCP1, UCP2 and ADRB3 genes influence weight loss in severely obese women submitted to hypocaloric dietary intervention. This longitudinal study included 21 women divided into two groups: Group 1 (Dietary intervention (G1)) consisted of 11 individuals with severe obesity (body mass index (BMI) ⩾40 kg/m2), selected for dietary intervention and Group 2 (Control (G2)) consisted of 10 normal-weight women (BMI between 18.5 and 24.9 kg/m2). Evaluation included weight (kg), height (m), waist circumference (cm), body composition, resting metabolic rate (RMR, kcal) and abdominal subcutaneous adipose tissue collection. The dietary intervention required that G1 patients remained hospitalized in the university hospital for 6 weeks receiving a hypocaloric diet (1200 kcal per day). The statistical analyses included t-test for paired samples, Spearman correlation and multivariate linear regressions, with the level of significance set at P

Introduction: obesity is associated with high levels of oxidative stress (OS) and inflammation. There is a lot of evidence that some polyphenols, such as green tea, have a positive impact on the OS state and consecutively, on inflammation. Objectives: the purposes of this study were: a) evaluate OS biomarkers in both obese and normal weight women; and b) evaluate if green tea supplementation has an impact on OS and inflammatory cytokine biomarkers of obese women. Methods: we evaluated obese (body mass index [BMI] ≥ 40 kg/m²) and normal weight (BMI between 18.5 and 24.9 kg/m²) women. Blood samples were used to access malondialdehyde (MDA), trolox equivalent antioxidant capacity (TEAC) and inflammatory cytokines. We randomly chose obese patients (18 individuals) and then gave them green tea supplementation for eight weeks. Statistical analysis included the Shapiro-Wilk, Wilcoxon, independent and paired t tests; p0.05 were considered as significant. Results: we enrolled 42 obese (BMI: 48.2 ± 9.3kg/m2) and 21 normal weight (BMI: 22.5 ± 2 kg/m2) women with an average age of 36.2 ± 9.1 years old. The serum levels of MDA were higher in obese (2.52 ± 0.31 µmol/l) than in eutrophic women (2.13 ± 0.26 µmol/l; p = 0.000). On the other hand, lower TEAC values were observed in the obese (0.75 ± 0.06 mM/l) than in the eutrophic group (0.78 ± 0.04 mM/l; p = 0.009). After the green tea intervention, MDA decreased 4.7% and TEAC increased 10%. Interleukin-6 (IL-6) serum levels decreased 12.7% after treatment (p = 0.03). Conclusions: a) the obese group had lower antioxidant capacity than eutrophic; and b) green tea supplementation ameliorated TEAC and MDA and reduced serum levels of IL-6 in obese women.Introducción: la obesidad se asocia con altos niveles de estrés oxidativo (EO) e inflamación. Existe mucha evidencia de que algunos polifenoles, como el té verde, tienen un impacto positivo en el estado del EO y, consecutivamente, en la inflamación. Objetivos: los propósitos de este estudio fueron: a) evaluar los biomarcadores de EO en mujeres obesas y de peso normal; y b) evaluar si la suplementación con té verde tiene un impacto en el EO y biomarcadores de citoquinas inflamatorias de las mujeres obesas. Métodos: evaluamos mujeres obesas (índice de masa corporal [IMC] ≥ 40 kg/m²) y con peso normal (IMC entre 18,5 y 24,9 kg/m²). Se utilizaron muestras de sangre para determinar el malondialdehído (MDA), la capacidad antioxidante equivalente de trolox (TEAC) y las citoquinas inflamatorias. Elegimos al azar pacientes obesas (18 individuos) y luego les dimos suplementos de té verde durante ocho semanas. El análisis estadístico incluyó las pruebas de Shapiro-Wilk, Wilcoxon, t pareadas e independientes; p0,05 fueron considerados como significativos. Resultados: se reclutaron 42 mujeres obesas (IMC: 48,2 ± 9,3 kg/m2) y 21 de peso normal (IMC: 22,5 ± 2 kg/m2) con un promedio de edad de 36,2 ± 9,1 años. Los niveles séricos de MDA fueron más altos en las personas obesas (2,52 ± 0,31 µmol/L) que en las mujeres eutróficas (2,13 ± 0,26 µmol/L; p = 0,000). Por otro lado, se observaron valores TEAC más bajos en los obesos (0,75 ± 0,06 mM/L) que en el grupo eutrófico (0,78 ± 0,04 mM/L; p = 0,009). Después de la intervención con té verde, la MDA disminuyó 4.7% y el TEAC aumentó 10%. Los niveles séricos de interleucina-6 (IL-6) disminuyeron 12.7% después del tratamiento (p = 0,03). Conclusiones: a) mujeres obesas tienen menor capacidad antioxidante que las eutrófica; y b) la suplementación con té verde mejora TEAC y MDA y redujo los niveles séricos de IL-6 en mujeres obesas.

Objectives Genetic predisposition and epigenetic signatures could explain why some individuals regain the weight lost after different obesity treatments. Major facilitator superfamily domain 3 (MFSD3) is a family of membrane-bound solute carriers whose expression has been recently associated with nutrient intake and adipose tissue homeostasis. This study aimed to evaluate a possible association between MFSD3 preoperative methylation pattern and weight regain after bariatric surgery. Methods This is a longitudinal study comprising 24 obese (body mass index > 35 m/kg2) women submitted to gastric bypass. Anthropometric measurements were evaluated at preoperative time and 1, 2, and 3 y after surgery, and then weight regain was calculated. Genomic DNA was extracted from leukocytes and was bisulfite modified by specific kits, according manufacturer's instructions. Methylation analysis was performed with the Infinium Human Methylation 450 K bead chip technology, and methylation level was expressed as a β value ranging from 0 (unmethylated) to 1 (fully methylated). Shapiro-Wilk, repeated-means analysis of variance, Spearman correlation, Mann-Whitney, and independent t tests were used in statistical analysis (P Results A total of 25% of patients regained significant weight. Weight regain after bariatric surgery was positively correlated with cg00010266 MFSD3 preoperative methylation levels (r = 0.6804, P = 0.0126). Moreover, cg00010266 MFSD3 baseline methylation levels were significantly higher in regainer patients than non-regainers (6.2 ± 1.5 versus 3.9 ± 1.2%, P = 0.026). Patients allocated in the higher cg00010266 MFSD3 preoperative methylation group had higher weight regain (4.1 ± 1.8 versus 6.7 ± 2.2 kg, P = 0.037). Conclusions Preoperative hypermethylation of MFSD3 gene is significantly associated with weight regain and a worse response to gastric bypass.

CONCLUSION The COVID-19 pandemic is a significant global public health challenge, especially concerning the pursuit of effective drugs for its prevention and treatment. Considering the prevalence of obesity worldwide and the complications associated with excessive body mass ratio, special attention should be given to patients with obesity. In a condition of obesity, reduced TAS2R expression could affect the response to medications such as CQ. Altogether, we highlighted the importance of obese patient care, particularly during the current COVID-19 pandemic. […] [...]

Introduction: inflammation and oxidative stress are factors that may play a substantial role in telomere attrition. In line of this, obesity is associated with telomere shortening. Green tea had anti-inflammatory and antioxidant effects and may alter telomere length (TL). Objectives: we evaluated the effect of decaffeinated green tea supplementation in obese women on TL. Methods: we conducted a cross-sectional interventional study with ten obese (body mass index [BMI] > 40 kg/m²) and eight normal weight (BMI > 18.5 and < 24.9 kg/m²) women (age between 27 and 48 years). The supplementation was carried out with capsules (each contained 450.7 mg of epigallocatechin-3-gallate) during eight weeks. Anthropometric and dietary intake assessment, and blood collection (for biochemical and TL analysis by quantitative PCR) were performed before and after supplementation. Normal weight patients were evaluated at a single moment. Results: we observed a significant increase on TL after supplementation (1.57 ± 1.1 to 3.2 ± 2.1 T/Sratio; p < 0.05). Moreover, we found shorter TL in obese patients (day 0) when compared to normal weight individuals (3.2 ± 1.9 T/Sratio; p < 0.05) and an inverse association between TL and BMI, even after age adjustment (beta = -0.527; r² = 0.286; IC = -0.129, -0.009). Conclusion: obesity is related to shorter telomeres. Green tea supplementation during eight weeks promotes telomere elongation in obese women.

This study aims (i) to verify expression of the UCPs, PLIN1, PPARG2, and ADRB3 genes in the abdominal subcutaneous adipose tissue of obese women at baseline and after 8 weeks of supplementation with decaffeinated green tea extract, and (ii) to associate findings with clinical parameters. This is a longitudinal study during which 11 women with obesity grade III were submitted to supplementation with 450 mg of (-)-epigallocatechin gallate (EGCG) (intervention group); the control group consisted of 10 eutrophic women. Anthropometric parameters [weight, height, and body mass index (BMI)], resting metabolic rate (RMR, measured by indirect calorimetry), and gene expression (measured by real-time PCR, RT-qPCR) were determined before and after supplementation. After 8 weeks, clinical parameters and UCP1, PLIN1, PPARG2, and ADRB3 expression remained unaltered in the intervention group (p .05). Genetic analysis also showed that the UCP3 gene was upregulated (p = .026), but its upregulation did not promote weight loss.

After bariatric surgery, modifications to signaling pathway networks including those of the metabolic regulator called mammalian or mechanistic target of rapamycin (mTOR) may lead to molecular alterations related to energy source availability, systemic nutrients, and catabolic and anabolic cellular processes. This study aimed to identify gene expression changes with regard to the mTOR complex 2 subunit signaling pathway in obese patients before and after bariatric surgery.The experimental group included 13 obese women who were examined before (preoperative) and 6 mo after (postoperative) Roux-en-Y gastric bypass (RYGB) surgery. The control group included nine apparently eutrophic women matched by age and without any other metabolic diseases (i.e., no diabetes and no liver or kidney diseases). Peripheral blood mononuclear cell samples were collected for RNA extraction and subsequent microarray analysis.After this methodological procedure, we identified 47 000 differentially expressed genes. A subsequent bioinformatic analysis showed that three diferentially expressed genes (rapamycin-insensitive companion of mTOR [RICTOR], phosphoinositide-3-kinase regulatory subunit 1 [PIK3 R1], and hypoxia inducible factor 1 alpha subunit 1A [HIF1 A]) participated in the mTOR signaling pathway. Real-time quantitative polymerase chain reaction revealed that RICTOR, PIK3 R1, and HIF1 A were upregulated 6 mo after RYGB surgery (P 0.05). In addition, patients in the experimental group lost weight significantly and presented significant improvement in biochemical/metabolic variables.The weight loss that was induced by RYGB surgery alters the mTOR signaling pathway and specifically the mTOR complex 2 subunit. The increased expression of genes that act in this pathway such as RICTOR, PIK3 R1, and HIF1 A reflects the induced weight loss and improved metabolic indicators (e.g., insulin resistance and lipolysis) that are evidenced in this study.

espanolIntroduccion: la obesidad se asocia con altos niveles de estres oxidativo (EO) e inflamacion. Existe mucha evidencia de que algunos polifenoles, como el te verde, tienen un impacto positivo en el estado del sistema operativo y consecutivamente en la inflamacion. Objetivos: los propositos de este estudio fueron: a) acceso a biomarcadores de EO en mujeres obesas y de peso normal; y b) evaluar si la suplementacion con te verde tiene impacto en los biomarcadores de citoquinas inflamatorias y de EO de mujeres obesas. Metodos: evaluamos mujeres obesas (indice de masa corporal - IMC ≥ 40 kg/m²) y peso normal (IMC entre 18,5 y 24,9 kg/m²). Se utilizaron muestras de sangre para acceder al malondialdehido (MDA), la capacidad antioxidante equivalente de Trolox (TEAC) y las citoquinas inflamatorias. Elegimos al azar pacientes obesos (18 individuos) y luego les dimos suplementos de te verde durante 8 semanas. El analisis estadistico incluyo las pruebas de Shapiro-Wilk, Wilcoxon, t pareadas e independientes, p Resultados: se reclutaron 42 mujeres obesas (IMC: 48,2 ± 9,3 kg/m2) y 21 de peso normal (IMC: 22,5 ± 2 kg/m2) con una edad promedio de 36,2 ± 9,1 anos. Los niveles sericos de MDA fueron mas altos en las personas obesas (2,52 ± 0,31 μmol/L) que en las mujeres eutroficas (2,13 ± 0,26 μmol/L; p = 0.000). Por otro lado, se observaron valores de TEAC mas bajos en obesos (0,75 ± 0,06 mM) que en el grupo eutrofico (0,78 ± 0,04 mM; p = 0,009). Despues de la intervencion del te verde, la MDA disminuyo 4,7% y el TEAC aumento 10%. Los niveles sericos de interleucina-6 (IL-6) disminuyeron 12,7% despues del tratamiento (p = 0,03). Conclusiones: el grupo obeso tenia menor capacidad antioxidante que el eutrofico. La suplementacion con te verde mejoro TEAC y MDA y redujo los niveles sericos de IL-6 en mujeres obesas. EnglishIntroduction: epigallocatechin-3-gallate (EGCG) is the most abundant catechin contained in green tea (Camellia sinensis) and has been associated with anti-obesity and anti-cancer effects, but the exact molecular mechanisms remain elusive. In this context, this study was designed to improve the understanding of the EGCG anti-obesity and anti-cancer action. Objectives: this study was designed to examine the effects of EGCG on the expression of genes involved in obesity and cancer pathways in the peripheral blood mononuclear cells of obese women. Material and methods: this longitudinal interventional study enrolled eleven women with severe obesity that were submitted to eight weeks of green tea (decaffeinated green tea capsules with 450.7 mg of EGCG, two capsules/day) supplementation (intervention group) and ten eutrophic women as a control group. Weight (kg), body mass index (BMI, kg/m2), fat mass (kg) and gene expression (qPCR method) were assessed before and after supplementation. HIF1-alpha (HIF1-α), phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) and rapamycin-insensitive companion of mTOR (RICTOR) were selected as potential targets. Results: after supplementation, body weight (114.9 ± 14.3 versus 115 ± 13.8 kg), body mass index (44.1 ± 3.7 versus 44.1 ± 3.9 kg/m2) and fat mass (47.6 ± 3.3 versus 47.3 ± 3.4 kg) did not change. EGCG upregulated the RICTOR and HIF1-α expression, however, did not modify PI3K expression. Conclusion: this study demonstrated that EGCG has a potential role to obesity and cancer related to obesity control and can be used not only for the purpose of weight loss, but also for the improvement of obesity-related comorbidities.

Introduction: Gene expression analyses from peripheral blood mononuclear cells (PBMC) and white adipose tissue are conflicting. It seems that results from single tissue are not enough to explain how changes affect humans as a complex biological system. Objective: The aim of this study was to compare, from obesity subjects, PBMC and white adipose tissue gene expression that regulates adipogenesis (perilipin 1 [PLIN1], adrenoreceptor beta 3 [ADRB3] and peroxisome proliferator-activated receptor [PPARG2]) and the energy metabolism (uncoupling protein UCP1, UCP2 and UCP3) process. Methods: This study enrolled 35 obese patients, with a body mass index (BMI) > 40 kg/m2 (obesity group [OG]), and ten eutrophic health subjects, 18 > BMI > 24.9 kg/m2 (control group [CG]). Anthropometric and body composition data were assessed at recruitment using standardized protocols. Samples of peripheral blood and subcutaneous adipose tissue (biopsy) were collected to analyze gene expression by RT-qPCR technique. For statistical analysis, we used the Shapiro-Wilk test and Wilcoxon tests by the SPSS software version 20.0; a p < 0.05 significance level was adopted. Results: There were significant differences of PLIN1, ADRB3, PPARG2 and UCP3 expression between blood against adipose tissue samples, showing that these genes are upregulated in adipose tissue. UCP2 expression was upregulated in PBMC. Conclusion: The PLIN1, ADRB3, PPARG2 and UCP3 genes were preferentially expressed in adipose tissue. However, UCP2 was upregulated in PBMC, suggesting that this gene may be assessed in a peripheral blood cell, which is easily accessible, safe and practical.

Analysis of the expression of genes related to the energy metabolism can elucidate the understanding of physiological and genetic factors that contribute to obesity. This study aimed to evaluate the expression of genes and its influence on resting metabolic rate and weight loss in obese patients before and after bariatric surgery.This study was conducted on 23 women, who were divided into two groups: bariatric surgery (preoperative and 6 months after surgery) and control. Abdominal subcutaneous adipose tissue samples were collected to analyze the gene expression, and the resting metabolic rate (RMR) was measured by indirect calorimetry.Significant differences were observed in weight reduction (22 %, p = 0.01), BMI (22.5 %, p = 0.01), and RMR values (10.5 %, p = 0.01) after the bariatric surgery, while the weight-adjusted RMR increased (15.8 %, p = 0.01). Increased UCP2 expression after 6 months of Roux-en-Y gastric bypass (RYGB) as compared to preoperative period (0.764 to 1.268, p = 0.01) was observed. Analysis with weight-adjusted RMR as dependent variable revealed that UCP2 (rWe have demonstrated that after 6 months of bariatric surgery, there is significant increase in the UCP2 expression. Additionally, the expression of UCP2 and PLIN1 genes influences the resting metabolic rate in obese individuals and could predict the weight loss after bariatric surgery.

Background/Objective Uncoupling proteins (UCPs) are located in the inner membrane of mitochondria. These proteins participate in thermogenesis and energy expenditure. This study aimed to evaluate how UCP1 and UCP3 expression influences substrate oxidation and elicits possible changes in body composition in patients submitted to bariatric surgery. Subjects/Methods This is a longitudinal study comprising 13 women with obesity grade III that underwent bariatric surgery and 10 healthy weight individuals (control group). Body composition was assessed by bioelectrical impedance. Carbohydrate and fat oxidation was determined by indirect calorimetry. Subcutaneous adipose tissue was collected for gene expression analysis. QPCR was used to evaluate UCP1 and UCP3 expression. Results Obese patients and the control group differed significantly in terms of lipid and carbohydrate oxidation. Six months after bariatric surgery, the differences disappeared. Lipid oxidation correlated with the percentage of fat mass in the postoperative period. Multiple linear regression analysis showed that the UCP1 and UCP3 genes contributed to lipid and carbohydrate oxidation. Additionally, UCP3 expression was associated with BMI, percentage of lean body mass, and percentage of mass in the postoperative period. Conclusions UCP1 and UCP3 expression is associated with lipid and carbohydrate oxidation in patients submitted to bariatric surgery. In addition, UCP3 participates in body composition modulation six months postoperatively.