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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004264naa a2200325 4500
001oai:lup.lub.lu.se:d5041bb6-8657-412a-9321-774ac2cb97b0
003SwePub
008190524s1977 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/d5041bb6-8657-412a-9321-774ac2cb97b02 URI
024a https://doi.org/10.1042/bj16804832 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Florén, Claes-Henriku Lund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Gastro,Forskargrupper vid Lunds universitet,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups4 aut0 (Swepub:lu)med-cfl
2451 0a Binding, interiorization and degradation of cholesteryl ester labelled chylomicron remnant particles by rat hepatocyte monolayers
264 1b Portland Press,c 1977
300 a 11 s.
520 a 1. The cholesteryl ester of isolated chylomicron-remnant particles was efficiently degraded by hepatocyte monolayers. The degradation was sensitive to metabolic inhibitors. 2. With increasing amounts of remnant cholesteryl ester the rate of uptake approached saturation and conformed to a linear double-reciprocal plot. The V(max.) was determined as 80ng of cholesteryl ester/h per mg of protein and the apparent K(m) as 1.4mug of cholesteryl ester per mg of protein. The time course for the uptake and hydrolysis suggested that binding of particles to the cell surface preceded the degradation. 3. Cholesteryl esters of native chylomicrons were degraded to a much smaller extent and their presence had only a small inhibitory effect on the degradation of chylomicron remnants. Intestinal very-low-density lipoproteins were degraded somewhat faster than chylomicrons, and caused more inhibition of remnant degradation. Rat high-density lipoproteins inhibited the hydrolysis of remnant cholesteryl ester by up to 50%, but had less influence on the amount of cholesteryl ester that was bound to the cells. Serum decreased both the uptake and hydrolysis, whereas d=1.21 infranatant had no effect. 4. The cholesteryl ester hydrolysis after the uptake by the cells was inhibited by chloroquine and by colchicine. Only 28-36% of the unhydrolysed cholesteryl ester could be released from these cells by trypsin treatment, indicating that the major portion was truly intracellular. The particles that could be released from the cell surface by trypsin and those remaining in the medium had the same triacylglycerol/cholesteryl ester ratio as the added remnant particles. Significant amounts of denser particles were thus not formed during contact with the cell surface. 5. The presence of heparin, as well as preincubation of the cells with heparin, increased the uptake of chylomicron remnants. This effect was most marked in the presence of serum. A much smaller proportion of the other serum lipoproteins was taken up, and this proportion was not increased by heparin.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Andra medicinska och farmaceutiska grundvetenskaper0 (SwePub)301992 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Other Basic Medicine0 (SwePub)301992 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng
700a Nilsson, Åkeu Lund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Gastro,Forskargrupper vid Lunds universitet,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups4 aut0 (Swepub:lu)med-ani
710a Medicin, Lundb Sektion II4 org
773t The Biochemical journald : Portland Pressg 168:3, s. 483-494q 168:3<483-494x 0264-6021
856u http://dx.doi.org/10.1042/bj1680483y FULLTEXT
8564 8u https://lup.lub.lu.se/record/d5041bb6-8657-412a-9321-774ac2cb97b0
8564 8u https://doi.org/10.1042/bj1680483

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