Marcela Pinhel

Influence of Excess Weight Loss and Weight Regain on Biochemical Indicators During a 4-Year Follow-up After Roux-en-Y Gastric Bypass

BackgroundBariatric surgery produces a substantial weight loss and improves the comorbidities associated with obesity such as diabetes mellitus and dyslipidemia, although inability to lose weight or weight regain has been estimated to occur in 20xa0% of cases. The objective of the present study was to assess the influence of weight variations on biochemical indicators during a 4-year period after bariatric surgery.MethodsA 4-year retrospective longitudinal study was conducted on 138 patients with grade III obesity submitted to Roux-en-Y gastric bypass, with the assessment of anthropometric measurements and biochemical indicators. The patients were divided into two groups according to percent excess weight loss (%EWL): %EWLu2009>u200950xa0% and %EWLu2009<u200950xa0%, and into two groups according to weight regain: <10xa0% and >10xa0%. The Student t test for independent samples was used to assess the differences in biochemical indicators between groups (pu2009≤u20090.05).ResultsFour years after surgery, there was a weight loss of 49.4u2009±u200921.8xa0kg and %EWL of 61u2009±u200921.2xa0%, with 73.2xa0% (nu2009=u2009101) of the patients showing %EWL of 50xa0% or more. Significant weight regain occurred in 24.6xa0% of the sample. There was a difference in weight, BMI, total cholesterol, LDL-cholesterol, triglycerides, and albumin between patients with different %EWL. No difference in biochemical indicators was observed between subjects with and without regain.ConclusionFour years after surgery, greater %EWL was associated with a better lipid profile. In addition, weight regain did not change the biochemical indicators of this patient series.

UCP1 and UCP3 Expression Is Associated with Lipid and Carbohydrate Oxidation and Body Composition

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.

The Ala55Val and -866G>A polymorphisms of the UCP2 gene could be biomarkers for weight loss in patients who had Roux-en-Y gastric bypass

OBJECTIVEnThe aim of this study was to investigate whether the Ala55Val and -866G>A polymorphisms of the UCP2 gene are related to weight loss and changes in body composition after bariatric surgery performed by Roux-en-Y gastric bypass (RYGB).nnnMETHODSnThis longitudinal study enrolled obese patients submitted to RYGB. Data regarding weight (kg), body mass index (kg/m2), fat-free mass (FFM; kg), fat mass (kg), weight loss (kg and %), and percent excess weight loss were collected from both preoperative and 1-y postoperative medical records. Polymorphisms were genotyped by allelic discrimination using real-time polymerase chain reaction and TaqMan-predesigned single nucleotide polymorphism Genotyping Assay kits (Applied Biosystems, Foster City, CA, USA). The t test was used to compare variables between genotypes of each polymorphism to analyze the dominant and recessive models. Linear regression models were used to adjust the effects of initial weight, age, and sex on the variation of weight and body composition (Pxa0<xa00.05).nnnRESULTSnWe analyzed 150 severely obese individuals (age 47.2xa0±xa010.5xa0y; 80% women). Genotype analysis showed a greater prevalence of heterozygous GA (41.3%) for -866G>A polymorphism and CT (39.3%) for Ala55Val polymorphism. Individuals who carried the T (CT+TT) and A (GA+AA) mutated alleles for Ala55Val and -866G>A, respectively, showed a higher weight and FFM loss.nnnCONCLUSIONnThe mutated alleles T for Ala55Val and A for -866G>A polymorphism could be biomarkers of weight loss 1xa0y after RYGB.

Alpha-synuclein A53T mutation is not frequent on a sample of Brazilian Parkinson’s disease patients

INTRODUCTIONnThe pathogenesis of Parkinsons disease (PD) involves both genetic susceptibility and environmental factors, with focus on the mutation in the alpha-synuclein gene (SNCA).Objective To analyse the polymorphism SNCA-A53T in patients with familial PD (FPD) and sporadic PD (SPD).nnnMETHODnA total of 294 individuals were studied, regardless of sex and with mixed ethnicity. The study group with 154 patients with PD, and the control group included 140 individuals without PD. The genotyping of SNCA-A53T was performed by PCR/RFLP. Significance level was p < 0.05.nnnRESULTSnAmong all patients, 37 (24%) had FPD and 117 (75.9%) had SPD. The absence of SNCA-A53T mutation was observed in all individuals.nnnCONCLUSIONnSPD is notably observed in patients. However, the SNCA-A53T mutation was absent in all individuals, which does not differ controls from patients. This fact should be confirmed in a Brazilian study case with a more numerous and older population.

Green tea supplementation promotes leukocyte telomere length elongation in obese women

INTRODUCTIONninflammation 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).nnnOBJECTIVESnwe evaluated the effect of decaffeinated green tea supplementation in obese women on TL.nnnMETHODSnwe 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.nnnRESULTSnwe 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).nnnCONCLUSIONnobesity is related to shorter telomeres. Green tea supplementation during eight weeks promotes telomere elongation in obese women.

Green tea supplementation upregulates uncoupling protein 3 expression in severe obese women adipose tissue but does not promote weight loss

Abstract 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 450u2009mg 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 (pu2009>u2009.05). Genetic analysis also showed that the UCP3 gene was upregulated (pu2009=u2009.026), but its upregulation did not promote weight loss.

Acknowledgement to the Reviewers

Chris T. Bolliger, Tygerberg, South Africa Raphael Borie, Paris, France Piera Boschetto, Ferrara, Italy Gabriel T. Bosslet, Indianapolis, USA Louis-Philippe Boulet, Sainte-Foy, Canada A. Bourdin, Montpellier, France John Brannan, Sydney, Australia Joerg Brederlau, Berlin, Germany E.C. Breen, La Jolla, USA Fabienne Bregeon, Marseille, France Pilar Brito-Zeron, Barcelona, Spain Dunja Bruder, Braunschweig, Germany Guy G. Brusselle, Gent, Belgium Martin H. Brutsche, St. Gallen, Switzerland Antonio Bugalho, Lisbon, Portugal Janette Burgess, Camperdown, Australia Umberto Campia, Chicago, USA Giorgio Walter Canonica, Genova, Italy Andre Capderou, Le Plessis Robinson, France Gaetano Caramori, Ferrara, Italy Pierluigi Carratu, Bari, Italy Laura Carrozzi, Pisa, Italy C.R.F. Carvalho, Sao Paulo, Brazil Gian Luca Casoni, Forli, Italy Loris Ceron, Carbonera, Italy Stefania Cerri, Portland, USA Indranil Chakravorty, London, UK Rachel Chambers, London, UK Shi-Chuan Chang, Taipei, Taiwan Ling Chen, Baltimore, USA Alfredo Chetta, Parma, Italy Carlo Chezzi, Parma, Italy Prashant N. Chhajed, Mumbai, India Doo-Sup Choi, Rochester, USA Marco Matteo Ciccone, Bari, Italy Michal Ciurzynski, Warsaw, Poland Donald W. Cockcroft, Saskatoon, Canada Henri Colt, Irvine, USA Alison Condliffe, Cambridge, UK Marco Confalonieri, Trieste, Italy Claudius Conrad, Boston, USA Vittoria Conti, Rome, Italy Robalo Cordeiro, Coimbra, Portugal Massimo Corradi, Parma, Italy Raja Abboud, Vancouver, Canada Yossef Aelony, Rancho Palos Verdes, USA Michalis Agrafiotis, Magoula, Greece Khalid Al Shafi, London, UK Ghada Alsaleh, Illkirch, France Nicolino Ambrosino, Cisanello, Pisa, Italy Kayvan Amjadi, Ottawa, Canada Asha Anandiah, Boston, USA Stephan Andreas, Immenhausen, Germany Jouke T. Annema, Leiden, The Netherlands Katerina Antoniou, Heraklion, Greece Balazs Antus, Budapest, Hungary Juan Carlos Arevalo, Salamanca, Spain Christine Armbruster, Vienna, Austria Laurent Arnaud, Paris, France Hormoz Ashtyani, Hackensack, USA John D. Aubert, Lausanne, Switzerland Najib Ayas, Vancouver, Canada Imran Aziz, Wigan, UK Chung-Xue Bai, Shanghai, China Kristina Bailey, Omaha, USA Petros Bakakos, Athens, Greece Bruno Balbi, Veruno, Italy Ferran Barbe, Lleida, Spain Xavier Basagana Flores, Barcelona, Spain Sandip Basu, Bombay, India Salvatore Battaglia, Palermo, Italy Sevim Bavbek, Ankara, Turkey Gillian Beamer, Columbus, USA H.D. Becker, Heidelberg, Germany Jurgen Behr, Bochum, Germany Carolyn Behrendt, Duarte, USA Maria Belvisi, London, UK Norbert Berend, Glebe, Australia Gidon Berger, Haifa, Israel Robert Berkowitz, Hackensack, USA Nitin Bhatt, Columbus, USA Luca Bianchi, Lumezzane, Italy Andrea Bianco, Campobasso, Italy Semra Bilaceroglu, Izmir, Turkey Jose Blanquer, Valencia, Spain Alexander Blau, Berlin, Germany Konrad E. Bloch, Zurich, Switzerland

LEP -2548G>A Polymorphism of the Leptin Gene and Its Influence on the Lipid Profile in Obese Individuals

Background/Aim: We studied the molecular pathogenesis of obesity, involving complex interactions between environmental and genetic factors, with a focus on the leptin gene. It was our aim to characterize the LEP -2548G>A leptin polymorphism and lipid profile in obese and normal-weight individuals. Methods: A total of 212 individuals were divided into the study group including 136 obese patients (body mass index, BMI ≥30) and the control group with 76 normal-weight individuals (BMI >18.5 and ≤24.9). DNA was amplified by polymerase chain reaction and restriction fragment length polymorphism. The lipid profile was analyzed by enzymatic colorimetric methods. The level of significance was set at p < 0.05. Results: There was a prevalence of the GA genotype in both groups. However, comparative group analysis showed an association of the recessive model (AA+GA) with increased triglycerides (TG) and decreased high-density lipoprotein cholesterol (HDL-C) levels in the study group. Conclusion: This study did not confirm an association between obesity and the LEP -2548G>A polymorphism. However, AA+GA genotypes, in the presence of obesity, seem to contribute to a reduction in HDL-C and an increase in TG compared with normal-weight individuals. This should be confirmed in further studies.