Artigo Acesso aberto Produção Nacional Revisado por pares

Dietary fat and apolipoprotein genotypes modulate plasma lipoprotein levels in Brazilian elderly women

2009; Springer Science+Business Media; Volume: 337; Issue: 1-2 Linguagem: Inglês

10.1007/s11010-009-0313-0

ISSN

1573-4919

Autores

Roberta Paula, Vinícius Carius de Souza, Andréa L. Benedet, Elias Rosa de Souza, Juliana Oliveira de Toledo Nóbrega, Clayton Franco Moraes, Lucy Gomes, Clarice Sampaio Alho, Cláudia Córdova, Otávio Tolêdo Nóbrega,

Tópico(s)

Lipoproteins and Cardiovascular Health

Resumo

Studies show that genetic polymorphisms in apolipoproteins, which are in charge of lipid transport, predispose to atherogenic dyslipidemia. This study aimed to investigate the impact of apolipoprotein E, A5, and B genotypes and dietary intake on lipid profile in a sample of elderly women in Brazil. Two hundred and fifty-two women (60 years or older) living in the outskirts of the Brazilian Federal District underwent clinical and laboratory assessments to characterize glycemic and lipidemic variables, and also to exclude confounding factors (smoking, drinking, hormone replacement, cognitive impairment, physical activity). Three-day food records were used to determine usual dietary intake, whereas genotypic evaluations were in accordance to established methodologies. Genotype frequencies were consistent with the Hardy–Weinberg equilibrium. Prior to adjustment, individuals carrying the ε2 allele showed higher serum levels of triglycerides (P < 0.05) and VLDL (P < 0.005) compared to ε4 carriers, whereas LDL levels were considerably elevated in ε4 compared to ε2 carriers. In the presence of high intake of total fat or a low ratio of polyunsaturated to saturated fatty acid, ε4 carriers lost protection against hypertriglyceridemia. There was no association of the apolipoprotein A5 and B genotypes with lipidemic levels independently of the fat intake regimen. Results are suggestive of a dysbetalipoproteinemic-like phenotype in postmenopausal women, with remarkable gene–diet interaction.

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