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

Autor(es):Mostrar menos -

Ferreira-Julio, Maysa Araujo ^[1] ; Pinhel, Marcela Souza ^[2] ; Gomes Quinhoneiro, Driele Cristina ^[2] ; Nicoletti, Carolina Ferreira ^[2] ; Brandao, Antonio Carlos ^[1] ; Nonino, Carla Barbosa ^[2] ; Pinheiro, Jr., Sidney ^[1] ; Parenti Oliveira, Bruno Affonso ^[2] ; Gregorio, Michele Lima ^[1] ; Andrade, Days Oliveira ^[1] ; Cortes-Oliveira, Cristiana ^[2] ; Souza, Doroteia Silva ^[1]

Afiliação do(s) autor(es)

^[1] Med Sch Sao Jose do Rio Preto FAMERP, Dept Mol Biol, Sao Jose Do Rio Preto - Brazil

^[2] Univ Sao Paulo, Dept Internal Med, Fac Med Ribeirao Preto FMRP, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Nutrigenetics and Nutrigenomics; v. 7, n. 4-6, p. 225-231, 2014.
• Citações Web of Science: 3

Resumo

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. (C) 2015 S. Karger AG, Basel (AU)

• Processo FAPESP: 08/54059-8 - Apolipoproteina e como fator de risco para colelitiase apos cirurgia bariatrica na obesidade morbida
• Beneficiário: Dorotéia Rossi Silva Souza
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 13/12819-4 - Alterações genéticas, clínicas, bioquímicas e de variabilidade cardíaca na Obesidade grau III pré e pós-cirurgia bariátrica
• Beneficiário: Marcela Augusta de Souza Pinhel
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado