Abstract
Population assays have consistently shown that the HDL concentration is inversely related to the incidence of cardiovascular disease and plays a protective role that is far more important than LDL as a risk factor. Although the atherogenic mechanisms of LDL have been extensively exploited in vitro and in vivo, the precise antiatherogenic mechanisms attributed to HDL are incompletely understood. A likely possibility is its role on the reverse cholesterol transport system whereby cholesterol from peripheral tissues (including the arterial wall) is taken up by the liver and excreted in bile. Taking into account that the control of the cholesterol metabolism in the body ought to vary more as a function of HDL than of LDL, that blood monocytes reflect the rates of boy cholesterol synthesis, and that there is a direct relationship between the latter and the intestinal absorption of cholesterol, the present project aims at quantifying the influence of the plasma concentration of HDL and its subfractions on the whole body cholesterol economy measured as: 1) the expression of cell receptors that transport cholesterol across the membrane for export; 2) cell production of cholesterol and uptake of lipoproteins containing apoB; 3) plasma markers of cholesterol body synthesis and intestinal cholesterol absorption. These objectives are attained measuring the parameters that regulate cholesterol metabolism in freshly collected blood Iympho-monocytes and the plasma steroids that are markers of synthesis (Iathosterol/desmosterol) and of the intestinal absorption (phytosterols/cholestanol). These parameters will be related to the degree of carotid intimal thickness measured by echo-color Doppler ultrasonography. (AU)
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