Fruchart J C
SERLIA et Unité Inserm, Institut Pasteur, Lille.
Ann Pharm Fr. 1994;52(3):117-23.
The antiatherogenic HDLs are heterogeneous in terms both of hydrated density and of lipoprotein composition. The LpA-I and LpA-I: A-II particles seem to be different from a metabolic point of view, and LpA-I and LpA-IV are apparently the only ones involved in the antiatherogenic action of HDLs. Alcohol consumption causes an increase in LpA-I: A-II, but not in LpA-I. Specific HDL binding sites have been demonstrated in various tissues, including steroidogenic tissues, liver cells and peripheral cells. Apolipoproteins A-I, A-IV and A-II are possible ligands. After binding to the uptake site, HDLs allow cholesterol supply to the cells, on one hand, and the removal of cholesterol for "reverse cholesterol transport" from peripheral tissues to the liver on the other hand. In addition, the interaction of the various HDL subfractions can cause different metabolic effects: cholesterol efflux from the adipocytes of cholesterol-laden mice is influenced by the uptake of LpA-I and LpA-IV on receptors, while apolipoproteins A-II are antagonists for this effect.
具有抗动脉粥样硬化作用的高密度脂蛋白（HDL）在水合密度和脂蛋白组成方面均具有异质性。从代谢角度来看，LpA-I和LpA-I:A-II颗粒似乎有所不同，而且LpA-I和LpA-IV显然是仅参与HDL抗动脉粥样硬化作用的成分。饮酒会导致LpA-I:A-II增加，但不会使LpA-I增加。已在包括类固醇生成组织、肝细胞和外周细胞在内的各种组织中证实了特异性HDL结合位点。载脂蛋白A-I、A-IV和A-II可能是配体。与摄取位点结合后，HDL一方面使胆固醇供应到细胞，另一方面将胆固醇从外周组织“逆向胆固醇转运”至肝脏。此外，各种HDL亚组分之间的相互作用可导致不同的代谢效应：富含胆固醇小鼠的脂肪细胞中胆固醇流出受LpA-I和LpA-IV在受体上摄取的影响，而载脂蛋白A-II则是这种效应的拮抗剂。
