RESUMO
The purpose of this study was to investigate the effects of the 5-HTTLPR and brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms on self-reported Big Five personality traits and their facets in a population representative sample of adolescents. The sample consisted of both cohorts of the Estonian Children Personality Behaviour and Health Study, and personality data were collected during its second waves. The 5-HTTLPR and BDNF Val66Met polymorphisms were genotyped. The BDNF Val66Met had a significant effect on conscientiousness [F(1,807)=4.32, P=0.038]. We did not find effects of the 5-HTTLPR polymorphism on the main domains of personality, however, a gene×gene interaction on conscientiousness emerged -BDNF Val66Met Met-allele carriers with the 5-HTTLPR s/s genotype had by far the lowest scores in conscientiousness [F(2,803)=4.38, P=0.012]. In addition, we found genotype effects on some facet scales. In conclusion, the BDNF Val66Met genotype Met-allele carriers have lower conscientiousness, and this effect is increased in the 5-HTTLPR s/s individuals.
Assuntos
Substituição de Aminoácidos/genética , Fator Neurotrófico Derivado do Encéfalo/genética , Personalidade/genética , Polimorfismo de Nucleotídeo Único/genética , Regiões Promotoras Genéticas/genética , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Adolescente , Alelos , Feminino , Heterozigoto , Homozigoto , Humanos , MasculinoRESUMO
Brain-derived neurotrophic factor (BDNF) regulates food intake and energy metabolism. It has also been suggested that mutations in the human BDNF gene and its receptor TrkB account for disturbed eating and obesity. The Met-allele of the BDNF Val66Met polymorphism has been associated with eating disorders, but the underlying mechanism of its contribution is not known. We report herewith that the effect of BDNF Val66Met polymorphism on binge eating in adolescent girls is dependent on severe food restriction. The scores on EDI-2 Bulimia subscale were significantly higher in BDNF Met-allele carriers who made attempts to regulate their body weight by reducing their meal frequency or by starving. This finding may help to explain why some people develop binge eating in response to dieting and others do not.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/genética , Bulimia/genética , Predisposição Genética para Doença/genética , Metionina/genética , Polimorfismo de Nucleotídeo Único , Valina/genética , Adolescente , Análise de Variância , Peso Corporal/fisiologia , Bulimia/etiologia , Comportamento Alimentar/fisiologia , Feminino , Frequência do Gene , Genótipo , Humanos , Masculino , Fatores Sexuais , Inanição/complicações , Inanição/genéticaRESUMO
UNLABELLED: Recently, two single nucleotide polymorphisms at position 45 and 276 on the adiponectin gene (ADIPOQ) have been recognized as determinants of total adiponectin levels, insulin resistance, and risk for diabetes in various obese populations. OBJECTIVES: The aim of this study was to determine whether these two polymorphisms are indeed determinants in the development of metabolic disorders or whether they are secondary to other confounding factors. METHODS: To do so, we have selected 170 physically active adolescent girls (mean age, 14.03 ± 1.5 years and mean body mass index, 19.98 ± 2.5 kg/m²) devoid of any metabolic diseases or confounding factors, to better attribute any findings to genotype effects. Concentration of adiponectin, insulin, and glucose were determined from blood samples with appropriate kits. Body fat parameters were evaluated with dual-energy X-ray absorptiometry, and genotype was analyzed with DNA extracted from whole blood samples followed by polymerase chain reaction and electrophoresis to separate alleles. RESULTS: Neither single nucleotide polymorphism +45T/G nor +276G/T was related to homeostasis model assessment index or adiponectin levels; however, the presence of the G allele on site 45 favored a significant decrease in lean body mass compared with those who were T homozygous (TG:36.90/TT:41.07 kg, P < 0.05). CONCLUSIONS: Results suggest that the reported increase in the risk of diabetes in subjects that were G allele carriers at site 45 in obese populations compared with normal-weight populations can be linked instead to a change in muscle mass or the muscle itself present in this genotype group.
