O papel da lipemia pós-prandial na gênese da aterosclerose: particularidades do diabetes mellitus

Abstract

Atherosclerosis is a complex and multifactorial disease, which determines clinical events that cause significant morbidity-mortality, represented by acute myocardial infarction, angina and sudden death. It is associated with lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, altered matrix metabolism, among other disturbances. All these abnormalities are usual and more pronounced in diabetic patients, as well as in the post-prandial state. Among the coronary artery disease risk factors that are not usually employed in clinical practice in the whole population, postprandial hyperlipemia plays a major role, being a possible early marker of metabolic abnormalities and vascular dysfunction not yet seen in the fasting state. Recent results showed that post-oral lipid overload changes are negatively associated with endothelial dysfunction, and vascular reactivity abnormalities are strongly related to atherosclerosis progression and cardiovascular events. These abnormalities could disclose a lipid intolerance state that can be detected in apparently healthy subjects even before fasting abnormalities are seen. This review will deal with the pathophysiology changes involved in post-prandial hyperlipemia and its relationship with atherogenesis, with particular emphasis to diabetes mellitus.

Comparison of Postprandial Lipemia between Women who are on Oral Contraceptive Methods and Those who are not

“…The decreasing lipid clearance leads to the increasing exposure of endothelial cells to esterified lipoproteins, and such an exposure causes changes in vascular reactivity associated with the progression of atherosclerosis and cardiovascular events. In the postprandial state, the increasing elevation of triglycerides can cause not only endothelial dysfunction, but also the lower availability of nitric oxide and the increasing oxidative stress, and such changes are strongly involved in the genesis of atherosclerosis 13 .…”

“…The magnitude and the amplitude of PPL are multifactorial, usually being prolonged for men 7 , showing increasing tendency with age 8 , in carbohydrate-rich diets 9 , among smokers 10 and obese people 11 . It is less common in physically active individuals 12 and more present among diabetic 13 , 14 and dyslipidemic patients 15 .…”

The influence of weight excess on the postprandial lipemia in adolescents

“…Saturated fatty acids, with the exception of Stearic acid, increased the serum levels of all lipoproteins, particularly LDLc, since they reduce the synthesis and activity of the LDLc receptors by diminishing the expression of RNAm and membrane fluidity [29]. It has been suggested that the ingestion of saturated fat is the main dietary cause of elevation of plasma cholesterol [30]. A possible explanation for the absence of post-prandial elevation of LDLc and TC in the studied adolescents was the small quantity of saturated fatty acid used in the experiment (10.7% - 2.7 g/100 ml).…”

“…A possible explanation for the absence of post-prandial elevation of LDLc and TC in the studied adolescents was the small quantity of saturated fatty acid used in the experiment (10.7% - 2.7 g/100 ml). In addition, the quantity of polyunsaturated fatty acid used (28.6% - 7.2 g/100 ml), may have influenced the LDLc and HDLc levels, because not only do polyunsaturated fats reduce LDLc, but they also reduce HDLc, thus inducing greater lipid oxidation [30]. Monounsaturated fats are as effect in the reduction of TC as are polyunsaturated fats, however, without causing lipid oxidation and reduction in HDL concentrations.…”

Efeitos do exercício físico sobre o perfil lipídico e inflamatório de mulheres jovens em uso de contraceptivo oral combinado: protocolo de um estudo sequencial cruzado

“…Todas essas novas condições favorecem alterações trombolíticas, vasoconstrictoras, inflamatórias e lipídicas; que em combinação, podem promover uma série de injúrias cardiovasculares determinantes para a doença aterosclerótica 3,7,8 .…”