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1.
Clin Nutr ; 30(2): 234-8, 2011 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-20870316

RESUMO

BACKGROUND & AIMS: Endothelial nitric oxide synthase (eNOS) gene variations have been linked to a higher risk for cardiovascular diseases (CVD) by unknown mechanisms. Our aim was to determine if two single nucleotide polymorphisms (SNPs) located in NOS3 (E298D and i19342) interfere with microvascular endothelial function (MEF) and/or oxidative stress during the postprandial state. METHODS: MEF was assessed with laser Doppler flowmetry at baseline and 2, 4, 6 and 8 h after ingestion of a single fatty meal (60% fat, 15% proteins and 25% carbohydrates) by 40 healthy young males. Oxidative stress was measured by nitrites/nitrates and oxidized LDL (LDL-ox) concentrations in fasting and postprandial states. RESULTS: Postprandial MEF was impaired in the carriers of minor alleles of the SNPs (global mean 60.99% Vs 87.25%, p = 0.016 for i19342; 63.62% Vs 95.71%, p = 0.011 for E298D). Carriers of E298D showed a higher LDL-ox at fasting and postprandial measures, and lower nitrites/nitrates at fasting. CONCLUSIONS: Minor allele carriers for E298D and i19342 have an impaired postprandial MEF and increased oxidative stress. Our results both provide insight into the higher risk of CVD attributed to E298D and identify variants that affect MEF in a healthy population.


Assuntos
Endotélio/enzimologia , Ácidos Graxos/metabolismo , Óxido Nítrico Sintase Tipo III/genética , Polimorfismo de Nucleotídeo Único , Alelos , Análise de Variância , Doenças Cardiovasculares/enzimologia , Doenças Cardiovasculares/genética , LDL-Colesterol/análise , Genótipo , Humanos , Desequilíbrio de Ligação , Masculino , Estresse Oxidativo , Período Pós-Prandial , Fatores de Risco , População Branca
2.
Clín. investig. arterioscler. (Ed. impr.) ; 21(1): 11-16, ene.-feb. 2009. tab, graf
Artigo em Espanhol | IBECS (Espanha) | ID: ibc-59944

RESUMO

Introducción. La hemostasia es un proceso complejo que regula la integridad del lecho vascular. La dieta modula la concentración de ciertos marcadores de hemostasis, aunque no está claro si el grado de resistencia a la insulina influye en esta relación. Nuestro objetivo fue investigar si la sensibilidad a la insulina influye en la concentración en ayunas y posprandial de ciertos marcadores de hemostasia (factor VII coagulante [FVIIc]), en el activador tisular del plasminógeno (tPA) y en el inhibidor del activador del plasminógeno (PAI-1), independientemente de la dieta consumida.Métodos. Estudio con diseño aleatorizado y cruzado, en el que 20 varones sanos recibieron 3 dietas, durante 4 semanas cada una, ricas en ácidos grasos monoinsaturados (Medit), saturados (Occid) e hidratos de carbono enriquecida con N3 (HC/N3). Posteriormente, se distribuyó a los participantes en 2 grupos: HOMA elevado (HE) o HOMA bajo (HB), dependiendo de las medianas para cada período de dieta. Se extrajeron determinaciones de FVIIc, tPA y PAI-1 en ayunas y 4 h después de una comida con la misma composición grasa que la seguida en el período previo, y se compararon los 2 grupos anteriores (HB frente a HE).Resultados. Hemos encontrado una concentración mayor, tanto de tPA como de PAI-1, en ayunas en el grupo HE, en relación con el grupo HB. El tPA también mostró una concentración mayor en el posprandio en el grupo HE.Conclusión. Nuestros datos indican una activación mayor de la coagulación en varones jóvenes con un índice HOMA mayor a la mediana poblacional, independientemente de la composición de la dieta seguida (AU)


Background. Haemostasis is a complex process that regulates the integrity of the circulatory system. It has been shown that diet can modulate the concentration of some haemostatic markers, but it is not clear if there is regulation of haemostasis depending on insulin sensitivity. We investigated whether insulin sensitivity influences fasting and postprandial concentration of haemostatic markers (FVIIc, PAI-1, tPA). Methods. Twenty healthy young men were submitted to three dietary intervention periods (rich in monounsaturated, saturated or n3 fatty acids) for four weeks each. The participants were separated into two groups (High-HOMA or Low-HOMA) depending on the median for the HOMA score after each period. Fasting and postprandial samples were drawn for the determination of the haemostatic markers. Results. High-HOMA group showed higher tPA and PAI-1 concentration levels in the fasting state compared with Low-HOMA group (p < 9.05). The tPA mean was also higher in the postprandial determination in the High-HOMA group. The type of diet received did not affect these results.Conclusion. In our study, the participants with higher HOMA score had a higher fasting concentration of tPA and PAI-1, and a higher postprandial concentration of tPA compared with the Low-HOMA group. These data suggest a higher activation of the coagulation cascade in healthy people with a HOMA score greater than the median for each population (AU)


Assuntos
Humanos , Hemostasia/fisiologia , Resistência à Insulina/fisiologia , Gorduras na Dieta/farmacocinética , Valores de Referência , Gorduras Insaturadas/farmacocinética , Inativadores de Plasminogênio/análise
3.
Clín. investig. arterioscler. (Ed. impr.) ; 21(6): 281-286, nov.-dic. 2009. ilus, tab, graf
Artigo em Espanhol | IBECS (Espanha) | ID: ibc-89385

RESUMO

Introducción. El síndrome metabólico (SM) determina un estado proinflamatorio y protrombótico que contribuye al desarrollo de la enfermedad arteriosclerótica. La dieta y, particularmente, el tipo de grasa tienen un papel importante en la inflamación y, por lo tanto, en el desarrollo de este síndrome. Objetivo. Estudiar el efecto posprandial de diferentes dietas en la proteína C reactiva (PCR) en pacientes con SM. Métodos. Se aleatorizó a 39 pacientes con SM, del estudio LIPGENE, para recibir una de estas dietas: una rica en SFA, una rica en MUFA y dos dietas bajas en grasa y ricas en hidratos de carbono complejos, una de ellas con PUFA n-3 de cadena larga (1,24 g/día) y la otra con placebo. Antes y después de cada período de intervención dietética, los pacientes se sometieron a una sobrecarga grasa con iguales tipo y composición de grasa que la dieta consumida durante las 12 semanas. Se determinaron las concentraciones plasmáticas de PCR a las 0, 1, 2, 3, 4, 5, 6 y 8 h durante el estudio posprandial. Resultados. No se observaron diferencias significativas en las concentraciones plasmáticas de PCR, entre los pacientes que consumieron las cuatro dietas, en ninguno de los estudios posprandiales. Tras el consumo a largo plazo, cuando se comparó la fase preintervención con la postintervención, al estudiar el incremento del área bajo la curva de la PCR, se observó un aumento significativo en el grupo que consumió la dieta rica en SFA (p = 0,031). Conclusiones. El consumo a largo plazo de una dieta rica en SFA, y no de una rica en MUFA o pobre en grasa con/sin PUFA n-3, produce un aumento posprandial de la PCR en comparación con el consumo agudo, lo que indica un aumento a largo plazo de la respuesta inflamatoria en pacientes con SM que consumen una dieta rica en grasa saturada (AU)


Introduction. The metabolic syndrome (MS) promotes a proinflammatory and prothrombotic state that contributes to the development of atherosclerosis. The diet and particularly the type of fat, plays an important role in the inflammation and therefore in the development of this syndrome. Objective. To study the postprandial response of different diets on C-reactive protein in MS patients. Methods. Thirty nine patients with MS from the LIPGENE study were randomized to receive one of the following four diets over a period of 12 weeks: a diet rich in SFA, a diet rich in MUFA, and two low-fat, high complex carbohydrate diets, one of them supplemented with long chain n-3 PUFA (1.24 g/day) and the other with placebo. Previously (pre) and after (post) the dietary intervention period, patients consumed a fat meal with the same type and composition of fat as in the diet consumed during the 12 weeks. The C reactive protein (CRP) plasma concentration was determined before and 1, 2, 3, 4, 5, 6 and 8 h after the fat meal consumption. Results. No significant differences in CRP plasma levels were found among the patients who consumed each diet, neither in the pre- or post-intervention postprandial studies. Nevertheless, we did find that the differences in the area under the curve for the CRP during the postprandial state was significantly increased in the group who consumed the SFA-rich diet (p = 0.031), when compared the pre- and post-intervention postprandial studies owing to the long-term consumption of this diet, but not in the MUFA-rich or low fat with or without n-3 PUFA diet. Conclusions. The chronic intake of a SFA-rich diet, but not the MUFA-rich or low fat with or without long chain n-3 PUFA diet, produces a postprandial increase of the CRP plasma levels when compared with the acute intake, which suggests a long-term increase in the inflammatory response in patients with MS who consumed a SFA-rich diet (AU)


Assuntos
Humanos , Gorduras na Dieta/metabolismo , Proteína C-Reativa/análise , Síndrome Metabólica/fisiopatologia , Inflamação/fisiopatologia , Período Pós-Prandial
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