917 resultados para Lipoproteins, LDL
Resumo:
outros, importantes factores de risco. Os objectivos do presente estudo são: estimar a prevalência dos diabéticos na população de um posto de colheitas de um laboratório de análises clínicas; caracterizar sócio-demograficamente a população diabética; identificar a prevalência de fumadores na população diabética; determinar a prevalência de diabéticos com dislipidemia; caracterizar os factores de risco cardiovascular dos diabéticos em estudo; calcular a prevalência de diabéticos medicados controlados; caracterizar os medicamentos antidiabéticos utilizados. Trata-se de um estudo descritivo observacional e transversal. Aplicou-se um questionário por entrevista, confidencial e voluntário e registaram-se os resultados dos seguintes parâmetros: HbA1c, glicemia em jejum, colesterol total, HDL, LDL e triglicéridos durante dois meses a todos os diabéticos de um posto de colheitas. Dos 1693 utentes, 24% (406/1693) referiram ser diabéticos. Destes, 54 preencheram os critérios de inclusão. Trinta e quatro são homens.A maioria (40,7%) tem entre 55 e 64 anos e 88,9% (48/54) tem dislipidemia. Dos diabéticos medicados, 82% (41/50) não têm a diabetes controlada. O grupo terapêutico mais utilizado é o das biguanidas (69,9%). O estudo demonstra uma elevada prevalência de doentes diabéticos com factores de risco não controlados (dislipidemia e hiperglicemia). Programas de educação para a saúde transversais focados na promoção de estilos de vida saudáveis, tendo como base o laboratório de análises clínicas podem contribuir para o controlo dos factores de risco cardiovascular.
Resumo:
O colesterol foi isolado pela primeira vez, em 1784 e desde então tem-se realizado várias pesquisas, estudos e ensaios relacionados com o colesterol. Esta molécula tão importante no organismo humano é o principal factor responsável pela formação da placa aterosclerótica. Com a descoberta das estatinas e a sua posterior comercialização, houve uma melhoria significativa em relação à morbilidade e à mortalidade por doenças cardiovasculares. Apesar de serem largamente utilizadas para reduzir os níveis de colesterol LDL, as estatinas também apresentam efeitos pleiotrópicos, ou seja, efeitos independentes do seu efeito na síntese do colesterol. Apesar de haver vários estudos realizados sobre estes efeitos e de já serem conhecidos vários mecanismos pelos quais eles actuam, ainda há perguntas que precisam de resposta. Assim é necessário continuar os estudos sobre os efeitos pleiotrópicos das estatinas. Ao longo deste trabalho vai ser dada resposta a duas perguntas essenciais. Em primeiro lugar, o que justifica o papel fundamental das estatinas na terapêutica actual? E por último, que outras situações clínicas poderão as estatinas ajudar a resolver ou melhorar?
Resumo:
Considerando que a prática de exercício físico com uma intensidade pelo menos moderada melhora a capacidade funcional (Maines et al., 1997; Clara et al., 2002; Olney et al., 2006), a qualidade de vida (Leal et al., 2005; Azevedo & Leal, 2009; Flynn et al., 2009) e diminui os fatores de risco coronários (Maines et al., 1997; Squires & Hamm, 2007; Perk, 2009; Pimenta, 2010), propõe-se com o presente estudo analisar o efeito do exercício físico supervisionado, em fase ambulatório precoce, realizada na comunidade, ao nível da recuperação de doentes cardíacos. Método: Aplicar-se-á um estudo experimental, em doentes cardíacos de ambos os sexos, entre os 28 e os 80 anos. Atribuir-se-á particular ênfase às alterações induzidas pela aplicação do programa de exercício físico nos parâmetros bioquímicos (colesterol total, C-LDL, C-HDL, triglicéridos e glicose), na composição corporal (peso, índice de massa corporal, perímetro da cintura), na capacidade funcional (consumo de oxigénio pico –V02 pico, equivalente metabólico, duplo produto), no nível de atividade física, na ingestão alimentar e na qualidade de vida. O estudo terá uma duração superior a três meses, comparando dois grupos, um grupo submetido ao exercício físico supervisionado (ES) e outro aos cuidados usuais (CU), os quais serão alvo de duas avaliações (inicial e final), avaliando-se a média e o desvio-padrão para todas as variáveis em estudo e recorrendo-se aos testes não paramétricos e paramétricos, para um nível de significância de p< .05. Resultados: Foram elegidos 52 doentes, sendo que 22 participaram no grupo cuidados usuais (CU) e 30 no grupo exercício físico supervisionado (ES), observando-se que o grupo ES apresentou melhorias mais acentuadas quando comparadas com o grupo CU, ao nível dos seguintes indicadores: dispêndio de kcal/semana (+697.22% vs +320.20%); PC (-3.19% vs +5.85%); CT (-23.92% vs -9.29%), C-LDL (-32.52% vs -8.92%); total de kcal/dia ingeridas (-33,31% vs -2.58%); VO2 pico (+30.88% vs -3.57%); qualidade de vida geral (+53.86% vs +2.96%). Conclusão: Concluindo que o exercício físico multicomponente, inserido na fase de ambulatório precoce na comunidade, potencia a recuperação de doentes cardíacos influenciando positivamente os fatores de risco de progressão da doença coronária, a capacidade funcional e a qualidade de vida fundamentais para que o doente possa, pelos seus próprios meios, retomar a sua vida na comunidade.
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Loudess discomfort levels (LDLs) were gathered from three Washington University School of Medicine sites, for a total of 325 subjects (total ears=454). These levels were compared to mean LDLs reported by Pascoe (1988). The results revealed that the mean LDL measured at WUSM (ie., the IHAFF procedure) is significantly different that the LDL reported by Pascoe (1988).
Resumo:
Differences in whole-body lipid metabolism between men and women are indicated by lower-body fat accumulation in women but more marked accumulation of fat in the intra-abdominal visceral fat depots of men. Circulating blood lipid concentrations also show gender-related differences. These differences are most marked in premenopausal women, in whom total cholesterol, LDL-cholesterol and triacylglycerol concentrations are lower and HDL-cholesterol concentration is higher than in men. Tendency to accumulate body fat in intra-abdominal fat stores is linked to increased risk of CVD, metabolic syndrome, diabetes and other insulin-resistant states. Differential regional regulation of adipose tissue lipolysis and lipogenesis must underlie gender-related differences in the tendency to accumulate fat in specific fat depots. However, empirical data to support current hypotheses remain limited at the present time because of the demanding and specialist nature of the methods used to study adipose tissue metabolism in human subjects. In vitro and in vivo data show greater lipolytic sensitivity of abdominal subcutaneous fat and lesser lipolytic sensitivity of femoral and gluteal subcutaneous fat in women than in men. These differences appear to be due to fewer inhibitory alpha adrenergic receptors in abdominal regions and greater a adrenergic receptors in gluteal and femoral regions in women than in men. There do not appear to be major gender-related differences in rates of fatty acid uptake (lipogenesis) in different subcutaneous adipose tissue regions. In visceral fat rates of both lipolysis and lipogenesis appear to be greater in men than in women; higher rates of lipolysis may be due to fewer alpha adrenergic receptors in this fat depot in men. Fatty acid uptake into this depot in the postprandial period is approximately 7-fold higher in men than in women. Triacylglycerol concentrations appear to be a stronger cardiovascular risk factor in women than in men, with particular implications for cardiovascular risk in diabetic women. The increased triacylglycerol concentrations observed in women taking hormone-replacement therapy (HRT) may explain the paradoxical findings of increased rates of CVD in women taking HRT that have been reported from recent primary and secondary prevention trials of HRT.
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There is currently considerable interest in potential atherogenic and thrombogenic consequences of elevated concentrations of triacylglycerols, especially in the post-prandial state. Despite this, there is limited information on the effects of dietary fatty acids on the synthesis, secretion and metabolism of chylomicrons, the large triacylglycerol-rich lipoproteins synthesized in the enterocyte following the digestion and absorption of dietary fat. This brief review considers current approaches to the investigation of chylomicron synthesis and summarizes some of the human, cell and animal studies that have investigated effects of different fatty acids on these pathways. Potential sites for modulatory effects of dietary fatty acids on the molecular events of chylomicron synthesis are proposed in the light of the recent model that has been developed from cell and animal studies and observations based on abnormalities in chylomicron formation in human inherited autosomal recessive diseases.
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The oxidised low density lipoprotein (LDL) hypothesis of atherosclerosis proposes that LDL undergoes oxidation in the interstitial fluid of the arterial wall. We have shown that aggregated (vortexed) nonoxidised LDL was taken up by J774 mouse macrophages and human monocyte-derived macrophages and oxidised intracellularly, as assessed by the microscopic detection of ceroid, an advanced lipid oxidation product. Confocal microscopy showed that the ceroid was located in the lysosomes. To confirm these findings, J774 macrophages were incubated with acetylated LDL, which is internalised rapidly to lysosomes, and then incubated (chase incubation) in the absence of any LDL. The intracellular levels of oxysterols, measured by HPLC, increased during the chase incubation period, showing that LDL must have been oxidised inside the cells. Furthermore, we found that this oxidative modification was inhibited by lipid-soluble antioxidants, an iron chelator taken up by fluid-phase pinocytosis and the lysosomotropic drug chloroquine, which increases the pH of lysosomes. The results indicate that LDL oxidation can occur intracellularly, most probably within lysosomes.
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It has previously been shown that experimental infections of the parasitic trematode Schistosoma mansoni, the adult worms of which reside in the blood stream of the mammalian host, significantly reduced atherogenesis in apolipoprotein E gene knockout (apoE(-/-)) mice. These effects occurred in tandem with a lowering of serum total cholesterol levels in both apoE(-/-) and random-bred laboratory mice and a beneficial increase in the proportion of HDL to LDL cholesterol. To better understand how the parasitic infections induce these effects we have here investigated the involvement of adult worms and their eggs on lipids in the host. Our results indicate that the serum cholesterol-lowering effect is mediated by factors released from S. mansoni eggs, while the presence of adult worms seemed to have had little or no effect. It was also observed that high levels of lipids, particularly triacylglycerols and cholesteryl esters, present in the uninfected livers of both random-bred and apoE(-/-) mice fed a high-fat diet were not present in livers of the schistosome-infected mice. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
Resumo:
A mathematical model describing the uptake of low density lipoprotein (LDL) and very low density lipoprotein (VLDL) particles by a single hepatocyte cell is formulated and solved. The model includes a description of the dynamic change in receptor density on the surface of the cell due to the binding and dissociation of the lipoprotein particles, the subsequent internalisation of bound particles, receptors and unbound receptors, the recycling of receptors to the cell surface, cholesterol dependent de novo receptor formation by the cell and the effect that particle uptake has on the cell's overall cholesterol content. The effect that blocking access to LDL receptors by VLDL, or internalisation of VLDL particles containing different amounts of apolipoprotein E (we will refer to these particles as VLDL-2 and VLDL-3) has on LDL uptake is explored. By comparison with experimental data we find that measures of cell cholesterol content are important in differentiating between the mechanisms by which VLDL is thought to inhibit LDL uptake. We extend our work to show that in the presence of both types of VLDL particle (VLDL-2 and VLDL-3), measuring relative LDL uptake does not allow differentiation between the results of blocking and internalisation of each VLDL particle to be made. Instead by considering the intracellular cholesterol content it is found that internalisation of VLDL-2 and VLDL-3 leads to the highest intracellular cholesterol concentration. A sensitivity analysis of the model reveals that binding, unbinding and internalisation rates, the fraction of receptors recycled and the rate at which the cholesterol dependent free receptors are created by the cell have important implications for the overall uptake dynamics of either VLDL or LDL particles and subsequent intracellular cholesterol concentration. (C) 2008 Elsevier Ltd. All rights reserved.
Resumo:
Background: The lipid-modulatory effects of high intakes of the fish-oil fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are well established and likely to contribute to cardioprotective benefits. Objectives: We aimed to determine the effect of moderate EPA and DHA intakes (< 2 g EPA + DHA/d) on the plasma fatty acid profile, lipid and apolipoprotein concentrations, lipoprotein subclass distribution, and markers of oxidative status. We also aimed to examine the effect of age, sex, and apolipoprotein E (APOE) genotype on the observed responses. Design: Three hundred twelve adults aged 20-70 y, who were prospectively recruited according to age, sex, and APOE genotype, completed a double-blind placebo-controlled crossover study. Participants consumed control oil, 0.7 g EPA + DHA/d (0.7FO), and 1.8 g EPA + DHA/d (1.8FO) capsules in random order, each for an 8-wk intervention period, separated by 12-wk washout periods. Results: In the group as a whole, 8% and 11% lower plasma triacylglycerol concentrations were evident after 0.7FO and 1.8FO, respectively (P < 0.001): significant sex x treatment (P = 0.038) and sex x genotype x treatment (P = 0.032) interactions were observed, and the greatest triacylglycerol-lowering responses (reductions of 15% and 23% after 0.7FO and 1.8FO, respectively) were evident in APOE4 men. Furthermore, lower VLDL-cholesterol (P = 0.026) and higher LDL-cholesterol (P = 0.010), HDL-cholesterol (P < 0.001), and HDL2 (P < 0.001) concentrations were evident after fish-oil intervention. Conclusions: Supplements providing EPA + DHA at doses as low as 0.7 g/d have a significant effect on the plasma lipid profile. The results of the current trial, which used a prospective recruitment approach to examine the responses in population subgroups, are indicative of a greater triacylglycerol-lowering action of long-chain n-3 polyunsaturated fatty acids in males than in females.
Resumo:
LDL oxidation may be important in atherosclerosis. Extensive oxidation of LDL by copper induces increased uptake by macrophages, but results in decomposition of hydroperoxides, making it more difficult to investigate the effects of hydroperoxides in oxidised LDL on cell function. We describe here a simple method of oxidising LDL by dialysis against copper ions at 4 degrees C, which inhibits the decomposition of hydroperoxides, and allows the production of LDL rich in hydroperoxides (626 +/- 98 nmol/mg LDL protein) but low in oxysterols (3 +/- 1 nmol 7-ketocholesterol/mg LDL protein), whilst allowing sufficient modification (2.6 +/- 0.5 relative electrophoretic mobility) for rapid uptake by macrophages (5.49 +/- 0.75 mu g I-125-labelled hydroperoxide-rich LDL vs. 0.46 +/- 0.04 mu g protein/mg cell protein in 18 h for native LDL). By dialysing under the same conditions, but at 37 degrees C, the hydroperoxides are decomposed extensively and the LDL becomes rich in oxysterols. This novel method of oxidising LDL with high yield to either a hydroperoxide- or oxysterol-rich form by simply altering the temperature of dialysis may provide a useful tool for determining the effects of these different oxidation products on cell function. (C) 2007 Elsevier Ireland Ltd. All rights reserved.
Resumo:
The in vitro antioxidant activity and the protective effect against human low density lipoprotein oxidation of coffees prepared using different degrees of roasting was evaluated. Coffees with the highest amount of brown pigments (dark coffee) showed the highest peroxyl radical scavenging activity. These coffees also protected human low-density lipoprotein (LDL) against oxidation, although green coffee extracts showed more protection. In a different experiment, coffee extracts were incubated with human plasma prior to isolation of LDL particles. This showed, for the first time, that incubation of plasma with dark, but not green coffee extracts protected the LDL against oxidation by copper or by the thermolabile azo compound AAPH. Antioxidants in the dark coffee extracts must therefore have become associated with the LDL particles. Brown compounds, especially those derived from the Maillard reaction, are the compounds most likely to be responsible for this activity.
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In this paper we report the antioxidant activity of different compounds which are present in coffee or are produced as a result of the metabolism of this beverage. In vitro methods such as the ABTS(center dot+) [ABTS = 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid)] decolorization assay and the oxygen radical absorbance capacity assay (ORAC) were used to assess the capacity of coffee compounds to scavenge free radicals. The importance of caffeine metabolites and colonic metabolites in the overall antioxidant activity associated with coffee consumption is shown. Colonic metabolites such as m-coumaric acid and dihydroferulic acid showed high antioxidant activity. The ability of these compounds to protect human low-density lipoprotein (LDL) oxidation by copper and 2,2'-azobis(2-amidinopropane) dihydrochloride was also explored. 1-Methyluric acid was particularly effective at inhibiting LDL oxidative modification. Different experiments showed that this caffeine metabolite is not incorporated into LDL particles. However, at physiologically relevant concentrations, it was able to delay for more than 13 h LDL oxidation by copper.
Resumo:
The oxidized low density lipoprotein (LDL) hypothesis of atherosclerosis proposes that LDL undergoes oxidation in the interstitial fluid of the arterial wall. We have shown that aggregated (vortexed) nonoxidized LDL was taken up by J774 mouse macrophages and human monocyte-derived macrophages and oxidized intracellularly, as assessed by the microscopic detection of ceroid, an advanced lipid oxidation product. Confocal microscopy showed that the ceroid was located in the lysosomes. To confirm these findings, J774 macrophages were incubated with acetylated LDL, which is internalized rapidly to lysosomes, and then incubated (chase incubation) in the absence of any LDL. The intracellular levels of oxysterols, measured by HPLC, increased during the chase incubation period, showing that LDL must have been oxidized inside the cells. Furthermore, we found that this oxidative modification was inhibited by lipid-soluble antioxidants, an iron chelator taken up by fluid-phase pinocytosis and the lysosomotropic drug chloroquine, which increases the pH of lysosomes. The results indicate that LDL oxidation can occur intracellularly, most probably within lysosomes.
Resumo:
Apolipoprotein A-IV (apoA-IV) inhibits lipid peroxidation, thus demonstrating potential anti-atherogenic properties. The aim of this study was to investigate how the inhibition of low density lipoprotein (LDL) oxidation was influenced by common apoA-IV isoforms. Recombinant wild type apoA-IV (100 mu g/ml) significantly inhibited the oxidation of LDL (50 mu g protein/ml) by 5 mu M CuSO4 (P < 0.005), but not by 100 mu M CuSO4, suggesting that it may act by binding copper ions. ApoA-IV also inhibited the oxidation of LDL by the water-soluble free-radical generator 2,2'-azobis(amidinopropane) dihydrochloride (AAPH; I mM), as shown by the two-fold increase in the time for half maximal conjugated diene formation (T-1/2; P < 0.05) suggesting it can also scavenge free radicals in the aqueous phase. Compared to wild type apoA-IV, apoA-IV-S347 decreased T-1/2 by 15% (P = 0.036) and apoA-IV-H360 increased T-1/2 by 18% (P = 0.046). All apoA-IV isoforms increased the relative electrophoretic mobility of native LDL, suggesting apoA-IV can bind to LDL and acts as a site-specific antioxidant. The reduced inhibition of LDL oxidation by apoA-IV-S347 compared to wild type apoA-IV may account for the previous association of the APOA4 S347 variant with increased CHD risk and oxidative stress. (c) 2006 Elsevier Ireland Ltd. All rights reserved.