Regulation of apolipoprotein A1 synthesis in lymph drained rats

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Fältnamn	Indikatorer	Metadata
000		04262naa a2200337 4500
001		oai:lup.lub.lu.se:3ec0c487-1066-4502-8dae-ea3ec38a9dc5
003		SwePub
008		190530s1987 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://lup.lub.lu.se/record/3ec0c487-1066-4502-8dae-ea3ec38a9dc52 URI
024	7	a https://doi.org/10.1016/0005-2760(87)90003-82 DOI
040		a (SwePub)lu
041		a engb engb swe
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a Franzen, Johan4 aut
245	1 0	a Regulation of apolipoprotein A1 synthesis in lymph drained rats
264	1	b Elsevier BV,c 1987
300		a 5 s.
520		a The effect of lymph diversion on plasma apolipoprotein A-I levels was studied. In lymph fistula rats apolipoprotein A-I levels in plasma stayed constant in spite of a loss of an equivalent of one-half plasma pool of apolipoprotein A-I per day through the lymph fistula. This indicates that synthesis of apolipoprotein A-I increases or that catabolism of apolipoprotein A-I decreases in a compensatory manner as intestinal apolipoprotein A-I is diverted. By using incorporation of [3H]leucine into newly synthesized apolipoprotein A-I it was shown that 2.6-times as much [3H]leucine was incorporated into apolipoprotein A-I in thoracic duct drained animals compared to controls. In experiments in which 125I-labeled HDL was injected intravenously into rats, it was shown that catabolism of HDL and apolipoprotein A-I was not decreased in lymph-drained rats. These data thus suggest that an increased synthesis of apolipoprotein A-I occurs when the intestinal contribution of apolipoprotein A-I diminishes. This is probably due to an increase in liver protein synthesis.
520		a The effect of lymph diversion on plasma apolipoprotein A-I levels was studied. In lymph fistula rats apolipoprotein A-I levels in plasma stayed constant in spite of a loss of an equivalent of one-half plasma pool of apolipoprotein A-I per day through the lymph fistula. This indicates that synthesis of apolipoprotein A-I increases or that catabolism of apolipoprotein A-I decreases in a compensatory manner as intestinal apolipoprotein A-I is diverted. By using incorporation of [3H]leucine into newly synthesized apolipoprotein A-I it was shown that 2.6-times as much [3H]leucine was incorporated into apolipoprotein A-I in thoracic duct drained animals compared to controls. In experiments in which 125I-labeled HDL was injected intravenously into rats, it was shown that catabolism of HDL and apolipoprotein A-I was not decreased in lymph-drained rats. These data thus suggest that an increased synthesis of apolipoprotein A-I occurs when the intestinal contribution of apolipoprotein A-I diminishes. This is probably due to an increase in liver protein synthesis.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Läkemedelskemi0 (SwePub)301032 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Medicinal Chemistry0 (SwePub)301032 hsv//eng
700	1	a 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
700	1	a 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
710	2	a Medicin, Lundb Sektion II4 org
773	0	t Biochimica et Biophysica Actad : Elsevier BVg 918:1, s. 11-15q 918:1<11-15x 0006-3002
773	0	t Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolismd : Elsevier BVg 918:1, s. 11-15q 918:1<11-15x 0005-2760
856	4	u http://dx.doi.org/10.1016/0005-2760(87)90003-8y FULLTEXT
856	4 8	u https://lup.lub.lu.se/record/3ec0c487-1066-4502-8dae-ea3ec38a9dc5
856	4 8	u https://doi.org/10.1016/0005-2760(87)90003-8

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