作者: Monique Mulder , Elly de Wit , Louis M. Havekes
DOI: 10.1016/0005-2760(91)90287-R
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摘要: It has been suggested that besides the LDL-receptor, hepatocytes possess an apo E or remnant receptor. To evaluate which hepatic lipoprotein receptor is involved in VLDL catabolism, we studied binding of remnants to HepG2 cells. Native was obtained from type IIb hyperlipidemic patients and treated with bovine milk lipase (LPL). This LPL-treated (LPL-VLDL) used as representative for remnants. Our results show LPL-VLDL binds high affinity Competition experiments showed 125I-labelled inhibited about 30% control value by simultaneous addition excess either unlabeled LDL LPL-VLDL. Preincubation cells resulted a reduction 34 55% value, whereas preincubation heavy HDL (density between 1.16 1.21 g/ml) stimulated 230% value. insulin (250 nM/l) also both (175 143% respectively). We conclude LDL-receptor no evidence presence on additional