作者: Bruce A. Griffin
DOI: 10.1079/PNS19990022
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摘要: Raised serum cholesterol does not adequately explain the increased risk of CHD within populations or relationship between diet and CHD. Nevertheless, principal transport vehicle in circulation, LDL, must still be regarded as most atherogenic lipoprotein species, but because its contribution to cholesterol. The potential LDL majority individuals arises from an increase number small dense particles content per se. There is now a wealth evidence cross-sectional prospective studies show that particle size significantly associated with predictive coronary risk. Moreover, there are credible mechanisms link process. rate influx lipoproteins into arterial wall function size, will thus more rapid for LDL. Components extracellular tissue matrix intima, notably proteoglycans, selectively bind high affinity, sequestering this pro-oxidative environment. oxidation promotes final deposition wall, numerous have shown susceptible oxidative modification than larger lighter counterparts. An may originate defect metabolism triacylglycerol-rich lipoproteins. One mechanism involve overproduction residence time large VLDL postprandial phase, situation thought arise through pathways insulin resistance.