Examinando por Autor "Kraft, Peter"
Mostrando 1 - 3 de 3
Resultados por página
Opciones de ordenación
Ítem Does genetic variation in the Δ6-desaturase promoter modify the association between α-linolenic acid and the prevalence of metabolic syndrome?(The American Journal of Clinical Nutrition, Vol.89, no. 3, 2009) Truong, Hong; DiBello, Julia R.; Ruiz Narváez, Edward A.; Kraft, Peter; Campos Núñez, Hannia; Baylin, AnaBackground: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are associated with protection against components of the metabolic syndrome, but the role of α-linolenic acid (ALA), the metabolic precursor of EPA and DHA, has not been studied. The Δ6-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the Δ6-desaturase gene (FADS2) may affect this conversion.Ítem Effect of apolipoprotein E genotype and saturated fat intake on plasma lipids and myocardial infarction in the Central Valley of Costa Rica(Human Biology, Vol. 79, no. 6, 2007) Yang, Yadong; Ruiz Narváez, Edward A.; Kraft, Peter; Campos, HanniaApolipoprotein E (apoE) is a ligand for the low-density lipoprotein (LDL) receptor and the LDL receptor-related protein (LRP) (Mahley and Rall 2000). Through these receptors apoE mediates the uptake of chylomicron remnants into the liver and the uptake of circulating very low density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) particles into peripheral tissues and cells (Mahley and Rall 2000).Ítem α-Linolenic acid, Δ6-desaturase gene polymorphism, and the risk of nonfatal myocardial infarction(The American Journal of Clinical Nutrition, Volumen 85, no. 2, 2007) Baylin, Ana; Ruiz Narváez, Edward A.; Kraft, Peter; Campos Núñez, HanniaBackground:Δ6-Desaturase (FADS2) is the rate-limiting step in the polyunsaturated fatty acid (PUFA) biosynthetic pathway. Objective: The aim was to test whether the common deletion [T/-] in the promoter of FADS2 affects the PUFA biosynthetic pathway and consequently modifies the effect of α-linolenic acid (ALA) on myocardial infarction (MI). Design: Case subjects (n =1694) with a first nonfatal acute MI were matched by age, sex, and area of residence to 1694 population-based control subjects in Costa Rica. PUFAs were quantified by gas-liquid chromatography from plasma and adipose tissue samples. Least-squares means from generalized linear models and odds ratios (ORs) and 95% CIs from multiple conditional logistic regression models were estimated. Results: The prevalence of the variant T/- allele was 48%. Eicosapentaenoic acid, γ-linolenic acid, and arachidonic acid decreased in adipose tissue and plasma with increasing number of copies of the variant allele with a monotonic trend (P < 0.05 for all). Fasting plasma triacylglycerols by genotype were 2.08 mmol/L for TT, 2.16 mmol/L for T-, and 2.26 mmol/L for - - [ie, homozygous for the variant (deletion) allele] (P = 0.03). The FADS2 deletion was not associated with MI and did not significantly modify the association between adipose tissue ALA and the risk of MI. Conclusions: The FADS2 deletion may prevent the conversion of ALA into very-long-chain PUFAs. However, this metabolic effect is not translated into an attenuated risk between ALA and MI among carriers of the variant. It is possible that, at current intakes of ALA, any potential defect in the transcription of the gene is masked by the availability of substrate. Further research in populations deficient in ALA intake is warranted.