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1.
Nutrition ; 70: 110499, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31655468

RESUMO

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 ß 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 < 0.05). 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.


Assuntos
Metilação de DNA/genética , Derivação Gástrica , Proteínas de Membrana Transportadoras/genética , Obesidade/genética , Aumento de Peso/genética , Adulto , Antropometria , Índice de Massa Corporal , Feminino , Predisposição Genética para Doença/genética , Humanos , Estudos Longitudinais , Pessoa de Meia-Idade , Obesidade/cirurgia , Período Pós-Operatório , Regiões Promotoras Genéticas , Fatores de Tempo , Resultado do Tratamento
2.
Nutr Hosp ; 35(3): 570-575, 2018 Jun 10.
Artigo em Inglês | MEDLINE | ID: mdl-29974764

RESUMO

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.


Assuntos
Catequina/análogos & derivados , Suplementos Nutricionais , Leucócitos/ultraestrutura , Obesidade/dietoterapia , Chá , Telômero/ultraestrutura , Adulto , Índice de Massa Corporal , Catequina/farmacologia , Estudos Transversais , Feminino , Humanos , Leucócitos/efeitos dos fármacos , Pessoa de Meia-Idade , Obesidade/sangue , Telômero/efeitos dos fármacos , Encurtamento do Telômero
3.
Nutr. hosp ; 35(3): 570-575, mayo-jun. 2018. graf, tab
Artigo em Inglês | IBECS | ID: ibc-180113

RESUMO

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


Introducción: la inflamación y el estrés oxidativo son factores que pueden jugar un papel importante en el desgaste de los telómeros. En línea con esto, la obesidad está asociada con el acortamiento de los telómeros. El té verde tiene efectos antiinflamatorios y antioxidantes y puede alterar la longitud de los telómeros (LT). Objetivos: evaluamos el efecto de la suplementación de té verde descafeinado en la LT en mujeres obesas. Métodos: realizamos un estudio intervencionista de corte transversal con 10 mujeres obesas (IMC > 40 kg/m²) y 8 con peso normal (IMC > 18,5 y < 24,9 kg/m²) (edad entre 27 y 48 años). La suplementación se llevó a cabo con cápsulas (cada una contenía 450,7 mg de epigalocatequina- 3-galato) durante 8 semanas. La evaluación de la ingesta antropométrica y dietética y la recolección de sangre (para análisis bioquímicos y LT por PCR cuantitativa) se realizaron antes y después de la administración de suplementos. Los pacientes de peso normal fueron evaluados en un solo momento. Resultados: observamos un aumento significativo en LT después de la suplementación (1,57 ± 1,1 a 3,2 ± 2,1 T/S ratio; p < 0,05). Además, encontramos LT más corta en pacientes obesos (día 0) en comparación con individuos de peso normal (3,2 ± 1,9 T/S ratio; p < 0,05) y una asociación inversa entre LT e IMC, incluso después del ajuste de edad (beta = -0,527; r² = 0,286; IC = -0,129, -0,009). Conclusión: la obesidad está relacionada con los telómeros más cortos. La administración de suplementos de té verde durante 8 semanas promueve la elongación de los telómeros en mujeres obesas


Assuntos
Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Catequina/análogos & derivados , Suplementos Nutricionais , Leucócitos/ultraestrutura , Obesidade/dietoterapia , Chá , Telômero/ultraestrutura , Índice de Massa Corporal , Catequina/farmacologia , Estudos Transversais , Leucócitos , Obesidade/sangue , Telômero , Encurtamento do Telômero
4.
Arq Neuropsiquiatr ; 71(7): 446-52, 2013 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-23857610

RESUMO

OBJECTIVE: This study aimed to analyze the frequency of GSTP1-Alw26I polymorphism and to estimate its association with toxic substances in Parkinson's disease (PD). METHODS: A study group with 154 patients - subdivided into familial and sporadic PD groups - and 158 elderly individuals without the disease (control group) were evaluated. GSTP1-Alw26I polymorphism was analyzed by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP). RESULTS: Patients were significantly more exposed to pesticides compared with the control group (p=0.0004), and the heterozygote genotype associated to exposure to pesticides also prevailed in patients (p=0.0001). Wild homozygote genotype was related to tobacco use (p=0.043) and alcoholism (p=0.033) in familial PD patients. CONCLUSION: Exposure to pesticides is associated to PD, whose effect can be enhanced when combined with the heterozygote genotype of GSTP1-Alw26I. Also, large genetic and environmental studies considering tobacco use, alcoholism, GSTP1 and PD are necessary to confirm our findings.


Assuntos
DNA-Citosina Metilases/genética , Glutationa S-Transferase pi/genética , Doença de Parkinson Secundária/induzido quimicamente , Doença de Parkinson Secundária/genética , Praguicidas/toxicidade , Polimorfismo Genético/genética , DNA Metiltransferases Sítio Específica (Adenina-Específica)/genética , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Feminino , Frequência do Gene , Heterozigoto , Humanos , Masculino , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase , Fatores de Risco , Fatores Sexuais
5.
Arq. neuropsiquiatr ; 71(7): 446-452, July/2013. tab, graf
Artigo em Inglês | LILACS | ID: lil-679164

RESUMO

Objective This study aimed to analyze the frequency of GSTP1-Alw26I polymorphism and to estimate its association with toxic substances in Parkinson's disease (PD). Methods A study group with 154 patients - subdivided into familial and sporadic PD groups - and 158 elderly individuals without the disease (control group) were evaluated. GSTP1-Alw26I polymorphism was analyzed by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP). Results Patients were significantly more exposed to pesticides compared with the control group (p=0.0004), and the heterozygote genotype associated to exposure to pesticides also prevailed in patients (p=0.0001). Wild homozygote genotype was related to tobacco use (p=0.043) and alcoholism (p=0.033) in familial PD patients. Conclusion Exposure to pesticides is associated to PD, whose effect can be enhanced when combined with the heterozygote genotype of GSTP1-Alw26I. Also, large genetic and environmental studies considering tobacco use, alcoholism, GSTP1 and PD are necessary to confirm our findings. .


Objetivo Analisar a frequência do polimorfismo GSTP1-Alw26I, assim como estimar sua associação com substâncias tóxicas na doença de Parkinson (DP). Métodos A casuística avaliada foi composta por um grupo de estudo, com 154 pacientes, subdivididos em DP familial e esporádica, e outro com 158 idosos sem a doença (grupo controle). O polimorfismo GSTP1-Alw26I foi analisado por reação em cadeia da polimerase/polimorfismo de comprimento do fragmento de restrição (PCR/RFLP). Resultados Os pacientes foram significativamente mais expostos a pesticidas, comparados com o grupo controle (p=0,0004), e o genótipo heterozigoto associado a exposição a pesticidas também prevaleceu nos pacientes (p=0,0001). O genótipo homozigoto selvagem apresentou relação com tabagismo (p=0,043) e etilismo (p=0,033) em pacientes com DP familial. Desse modo, a exposição a pesticidas está associada à DP, cujo efeito pode ser potencializado quando combinado ao genótipo heterozigoto de GSTP1-Alw26I. Estudos genético-ambientais envolvendo tabagismo, etilismo, GSTP1 e DP devem ser realizados em casuísticas numerosas, confirmando essa associação. .


Assuntos
Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , DNA-Citosina Metilases/genética , Glutationa S-Transferase pi/genética , Doença de Parkinson Secundária/induzido quimicamente , Doença de Parkinson Secundária/genética , Praguicidas/toxicidade , Polimorfismo Genético/genética , DNA Metiltransferases Sítio Específica (Adenina-Específica)/genética , Estudos de Casos e Controles , Frequência do Gene , Heterozigoto , Reação em Cadeia da Polimerase , Fatores de Risco , Fatores Sexuais
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