It had been found that Beijing ducks（BD） have a high level of HDL（70%）

high LCAT but very low CETP activity and will not develop atherosclerosis on an atherogenic diet

suggesting that cholesterol ester is mainly carried by HDL and metabolized through an HDL receptor pathway in the liver. However

evidence of this receptor′s existence in the liver is not yet complete. In this paper. the HDL receptor in BD liver has been studied. Our experiments showed : 1 ) ApoE-free 125 I-HDL could bind specifically to duck hepatic cell membrane with high affinity （Kd=9.6μg/ml） and was saturable （Bmax=8.9μg/mg cell membrane protein）at room temperature 2)Competitive inhibition studies with unlabelled duck

human

rat and chick HDL and duck apo AI and its liposomes formed with PC or DMPC could inhibit the binding of 125I-HDL to duck hepatic cell membranes

but LDL

apo E and their liposomes with PC or DMPC could not with the exception of duck LDL. 3) The receptor could recognize apo AI but not apo B or E. 4 ) Both phosphorase A2 and pronase could inhibit the binding activity. The above results give strong evidence for the existence of a specific HDL receptor pathway in the duck liver

supporting our hypothesis that CE in Beijing ducks is metabolized directly through the hepatic HDL receptor instead of being transfered back to VLDL and LDL

then through the LDL receptor pathway. This unique way of metabolizing CE may be behind the Beijing duck’s antiatherogenicity.