Obesity and insulin resistance are associated with an increase of cardiovascular risk factors, including adipocytokines. The aim of this study was to investigate the effect of low-calorie diet on serum lipids, adipokines, insulin resistance and body composition in obese women. It was a clinical trial with class I obese women aged 30-45 years submitted to hypocaloric diet for 90 days. Dietary intake, anthropometric parameters, body composition, serum lipids, glucose, insulin, leptin, adiponectin, HOMA-IR and QUICKI indexes were evaluated at the baseline, 30, 60 and 90 days. There was 30% significant decrease in energy intake, and also decrease in body weight, body mass index and waist circumference (p < 0.01) throughout the treatment period. Despite the amount of lean body mass (kg) reduced in average, it was observed that lean body mass (%) had increased (p < 0.01) and that the amount of fat body mass (kg) had decreased significantly in the third month (p < 0.05). Systolic blood pressure reduced up to -5mmHg (p < 0.05) after 90 days. Was observed a decrease (p < 0.05) on serum insulin and HOMA-IR until the 60th day, while the serum adiponectin increased (p < 0.01) during treatment. Corroborating with the reduction of fat body mass and weight, serum leptin also reduced (p < 0.01). These results suggest that the short-term low-calorie diet reduces total body fat, mainly found in the abdominal region, and efficiently improve insulin sensitivity decreasing cardiovascular risk in obese women.

La obesidad y la resistencia a la insulina se asocian con un aumento de los factores de riesgo cardiovascular, incluyendo las adipocitocinas. El propósito de este estudio fue investigar el efecto de una dieta baja en calorías sobre los lípidos séricos, las adipocinas, la resistencia a la insulina y la composición corporal en mujeres obesas. Se trataba de un estudio clínico en mujeres con obesidad de clase I, con edades entre 30-45 años, sometidas a una dieta hipocalórica durante 90 días. Se evaluaron basalmente y a los 30, 60 y 90 días la ingesta dietética, los parámetros antropométricos, la composición corporal, los lípidos séricos, la glucosa, la insulina, la leptina, la adiponectina y los índices HOMA-IR QUICKI. Hubo un descenso significativo del 30 % en el consumo de energía y un descenso del peso corporal, el índice de masa corporal y la circunferencia de la cintura (p < 0,01) durante todo el periodo de tratamiento. A pesar de que se redujo en promedio la masa magra corporal (kg), se observó que la masa magra corporal (%) se incrementó (p < 0,01) y que la cantidad de masa corporal grasa (Kg) disminuyó significativamente al tercer mes (p < 0,05). La presión sanguínea sistólica se redujo en 5 mmHg (p < 0,05) a los 90 días. Observamos un descenso de la insulina sérica y del HOMA-IR en el día 60 (p < 0,05), mientras que la adiponectina sérica aumentó (p < 0,01) durante el tratamiento. Como corroboración de la reducción de la masa corporal grasa y del peso, la leptina sérica también se redujo (p < 0,01). Estos resultados sugieren que la dieta hipocalórica a corto plazo reduce la grasa corporal total, fundamentalmente en la región abdominal y mejora de forma eficiente la sensibilidad a la insulina disminuyendo el riesgo cardiovascular en mujeres obesas.

Background: The metabolic syndrome is related to the increase in cardiovascular diseases. Polyunsaturated fatty acids from fish oil help in reducing cardiovascular risk factors and are natural bindings of PPARy2. Objective: To evaluate the impact of hypocaloric diet associated with microencapsulated fish oil supplementation in women with metabolic syndrome. Methods: We conducted a randomized, single-blind and placebo-controlled clinical trial with adult women who presented metabolic syndrome (n = 30) for 90 days. The volunteers were divided into two groups: placebo group (n = 15) and microencapsulated fish oil group (n = 15) (3 g/day of microencapsulated fish oil containing 0.41 g/day of eico-sapentaenoic acid and decosahexaneoic acid). Anthropometric, body composition, clinical and laboratory parameters were assessed before and after the intervention. Paired t-test was used for comparisons within groups and Student's t-test for comparison between groups. We considered p < 0.05 as significant values. Results: The comparison between groups revealed a significant reduction of blood glucose, insulinemia and the homeostasis model assessment in the microencapsulated fish oil group after 90 days, as opposed to the placebo group. We also observed reduction of the systolic arterial pressure in the microencapsulated fish oil group. Conclusion: A hypocaloric diet associated with the consumption of microencapsulated fish oil was effective in reducing blood glucose, insulinemia and insulin resistance in women with MS.

Antecedentes: El síndrome metabólico se relaciona con un incremento de las enfermedades cardiovasculares. Los ácidos grasos poliinsaturados del aceite de pescado ayudan a reducir los factores de riesgo cardiovascular y son ligandos naturales del PPARy2. Objetivo: Evaluar el impacto de la dieta hipocalórica asociada con suplementación de aceite de pescado micro-encapsulado en mujeres con síndrome metabólico. Métodos: Realizamos un ensayo clínico de distribución aleatoria, simple ciego y controlado con placebo en mujeres adultas con síndrome metabólico (n = 30) durante 90 días. Se dividió a las voluntarias en dos grupos: el grupo placebo (n = 15) y el grupo con aceite de pescado microencapsulado (n = 15) (3 g/día de aceite de pescado microencapsulado que contienen 0,41 g/día de ácido eicosapentaenoico y de ácido decosahexaneoico). Se evaluaron parámetros antropométricos, clínicos y de laboratorio y la composición corporal antes y después de la intervención. Se emplearon la prueba t pareada para las comparaciones dentro de los grupos y la prueba t de Student para la comparación entre grupos. Consideramos valores significativos de p < 0,05. Resultados: La comparación entre grupos reveló una reducción significativa de la glucosa sanguínea, la insulinemia y la evaluación del modelo homeostático en el grupo de aceite de pescado microencapsulado tras 90 días, en comparación con el grupo placebo. También observamos una reducción de la presión arterial sistólica en el grupo con aceite de pescado microencapsulado. Conclusión: La dieta hipocalórica asociada con el consumo de aceite de pescado microencapsulado fue eficaz en la reducción de la glucosa sanguínea, la insulinemia y la resistencia a la insulina en mujeres con SM.

Introduction: Glucose metabolism may be altered in obesity and genotype for PPAR 2 can influence this variable. Objective: To evaluate the influence of body mass (BM) and visceral adiposity (VA) in glucose metabolism in morbid obese women with Pro12Pro genotype. Methods: Were selected 25 morbidly obese women. Groups were formed according to body mass index (BMI) [G1: 40-45 kg/m² (n = 17); G2: > 45 kg/m² (n = 8)]. Anthropometric, glycemia and insulinemia assessments (fasting, 60 and 120 minutes after high polyunsaturated fatty acids meal) were carried out. The insulin resistance (IR) and insulin sensitivity (IS) were assessed by HOMA-IR and QUICKI respectively. Results: G2 had higher BMI and waist circumference, compared to G1, impaired fasting glucose, low IS and higher IR. The postprandial glucose was normal, but there was a higher insulin peak one hour after the meal in G2. Conclusion: Increased BM and VA were associated with worse glucose metabolism suggesting metabolic differences between morbid obese with Pro12Pro genotype.

Introducción: El metabolismo de la glucosa puede estar alterado en la obesidad y el genotipo del gene PPAR 2 puede influir en este variable. Objetivo: Evaluar la influencia de la masa corporal (MC) y de la adiposidad visceral (AV) en el metabolismo de la glucosa en mujeres con obesidad de grado 3 con el genotipo Pro12Pro. Métodos: Se seleccionaron 25 mujeres con obesidad de grado 3. Se formaron grupos de acuerdo con el índice de masa corporal (IMC) [G1: 40-45 kg/m² (n = 17), G2: > 45 kg/m² (n = 8)]. Fueron hechas evaluaciones antropométricas, de la glucemia y de la insulinemia (en ayunas, 60 y 120 minutos después de la comida rica en ácidos grasos poliinsaturados). La resistencia a la insulina (RI) y sensibilidad a la insulina (SI) fueron evaluados por el HOMA-IR y QUICKI, respectivamente. Resultados: G2 tuvieron mayor índice de masa corporal y circunferencia de la cintura, en comparación con G1, peor glucemia en ayunas, baja SI y alta RI. La glucosa postprandial fue normal, pero hubo un pico de insulina más alto una hora después de la comida en G2. Conclusión: El aumento de la MC y de la AV se asociaron con peor metabolismo de la glucosa lo que sugiere diferencias metabólicas entre obesos de grado 3 con el genotipo Pro12Pro.

A deficiência de ácido fólico está associada às doenças crônicas não-transmissíveis, complicações na gestação e doenças neurodegenerativas. Objetivou-se discutir o papel do ácido fólico na prevenção de doenças, os aspectos epidemiológicos de sua deficiência, fortificação dos alimentos e suplementação medicamentosa. Realizou-se levantamento bibliográfico, consultando as bases de dados para a obtenção dos artigos completos: MedLine, SciELO, PubMed, Highwire Press e Science Direct. Foram selecionados estudos realizados com seres humanos publicados entre 2004 e 2010. O ácido fólico é importante para as reações de metilação do ácido desoxirribonucléico, prevenção da hiper-homocisteinemia e atua como antioxidante. A deficiência dessa vitamina é descrita em adolescentes, mulheres em idade fértil, gestantes e em idosos. Seu alcance pela dieta é difícil, sendo necessária a inclusão de alimentos fortificados ou suplementos. É importante avaliar o estado nutricional de ácido fólico dos indivíduos antes e após a adoção dessas estratégias, de modo a gerar subsídios para ela-boração de medidas governamentais mais adequadas e eficazes. Destacamos ainda a necessidade da reeducação nutricional para a população brasileira a fim de aumentar o consumo de alimentos fontes de ácido fólico.

Folic acid deficiency is associated with non-communicable chronic diseases, pregnancy-associated complications and neurodegenerative diseases. The objective of this paper was to discuss the role of folic acid in disease prevention, the epidemiological aspects of its deficiency and food fortification and supplementation. Articles were searched in the following databases: MedLine, SciELO, PubMed, Highwire Press and Science Direct. Only original studies with humans published between 2004 and 2010 were included. Folic acid is important for DNA methylation and prevention of hyperhomocysteinemia. It also presents antioxidant activity. Folic acid deficiency has been described in adolescents, women of childbearing age, pregnant women and the elderly. It is difficult to meet the folic acid requirement with diet alone, so fortified foods and supplements are necessary. It is important to assess folic acid levels before and after the implementation of such strategies to enable the development of better and more effective public strategies. It is also important to provide nutrition education for the Brazilian population for them to increase their consumption of dietary sources of folic acid.

A hiper-homocisteinemia é um fator de risco independente para as doenças vasculares oclusivas. Os mecanismos exatos pelos quais a hiper-homocisteinemia favorece o desenvolvimento dessas doenças não são totalmente compreendidos. Sugere-se que o dano ao endotélio vascular, promovido pelas espécies de oxigênio reativas, oriundas da oxidação da homocisteína, seja a causa dos eventos tromboembólicos. Estudos indicam que a homocisteína interfere em vários mecanismos anticoagulantes mediados pelo endotélio vascular, tais como: redução da ativação da proteína C, inibição da trombomodulina e supressão da expressão do sulfato de heparan. Sabe-se que os níveis de homocisteína são influenciados por diversos fatores, dentre eles destaca-se a deficiência de vitaminas do complexo B (especialmente folato, cobalamina e piridoxina). A suplementação de folato, isoladamente ou em combinação com a cobalamina e piridoxina, reduz os níveis de homocisteína plasmática mesmo em pessoas que não apresentam deficiência dessas vitaminas. Esta revisão tem como objetivos abordar os possíveis mecanismos pelos quais a hiper-homocisteinemia poderia levar ao desenvolvimento de eventos tromboembólicos e o tratamento nutricional da hiper-homocisteinemia.

Hyper-homocysteinemia is an independent risk factor for occlusive vascular disease. The exact mechanisms by which hyperhomocysteinemia promotes the development of these diseases are still unclear. It has been suggested that damage to the vascular endothelium caused by reactive oxygen species produced during the auto-oxidation of homocysteine, may be the cause of the thrombo-embolic events. Studies have indicated that homocysteine interferes in various anticoagulant mechanisms mediated by the vascular endothelium, for example, reduction in protein C activation, inhibition of thrombomodulin and suppression of heparan sulfate expression. It is known that many factors influence the homocysteine levels including deficiency of the vitamin B complex (mainly folate, pyridoxine and cobalamin). Folate supplementation, alone or combined with pyridoxine and cobalamin, reduces plasmatic homocysteine levels even in people who are not vitamin deficient. This paper will address the possible mechanisms by which hyper-homocysteinemia could favor the development of thrombo-embolic events as well as addressing its nutritional treatment.