Metabolism of iodinated very low density lipoprotein in the rat

Stein, O.; Rachmilewitz, Daniel; Sanger, L.; Eisenberg, Shlomo; Stein, Y.

doi:10.1016/0005-2760(74)90170-2

Cited by 65 publications

(12 citation statements)

References 18 publications

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“…Therefore it is clear that the hepatic lipase is not taking part in the uptake of chylomicron remnants, since the enzyme is not located on parenchymal cells. Also the apoprotein moiety of very-low-density lipoprotein accumulates mainly in parenchymal cells (Stein et al, 1974), suggesting a similar catabolic pathway for these lipoproteins and for chylomicrons.…”

Section: Resultsmentioning

confidence: 95%

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Localization of the heparin-releasable lipase in situ in the rat liver

Kuusi¹,

Nikklä²,

Virtanen³

et al. 1979

Biochemical Journal

163

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Immunofluorescence and immuno-electron microscopy were used for the localization of the heparin-releasable lipase in situ in the rat liver. The lipase is located exclusively on the liver endothelial cells. No labelling could be detected on the parenchymal of Kupffer cells, or in the livers of heparin-pretreated animals. The physiological significance of the endothelial localization of the hepatic lipase is discussed.

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Section: Resultsmentioning

confidence: 95%

“…The functional significance of this finding is important. The different cell types in liver apparently metabolize different classes of lipoproteins (Stein & Stein, 1969;Stein et al, 1974;van Berkel et al, 1977;Andersen et al, 1977;van Berkel & van Tol, 1978).…”

Section: Resultsmentioning

confidence: 99%

Localization of the heparin-releasable lipase in situ in the rat liver

Kuusi¹,

Nikklä²,

Virtanen³

et al. 1979

Biochemical Journal

163

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“…The removal of VLDL-B in the rat also appears to be multiexponential (13). This may reflect the very rapid rate of removal of VLDL apoprotein from the plasma coupled to the much slower rate of uptake and catabolism of remnants in the liver (14,36).…”

Section: Discussionmentioning

confidence: 99%

“…While it is highly probable that the catabolism of VLDL takes place largely within the plasma, lipoproteins resembling VLDL have been identified in human lymph (37). Catabolism of VLDL remnants has been described in several tissues (14,36,38), and VLDL-B can be degraded in a variety of cultured cells2 (39). The presence of VLDL-like par-ticles in the intestine (40) represents another possible pool of VLDL that might exchange with the intravascular pool.…”

Section: Discussionmentioning

confidence: 99%

Catabolism of Very Low Density Lipoprotein B Apoprotein in Man

Reardon¹,

Fidge²,

Nestel³

1978

J. Clin. Invest.

222

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A B S T R A C a The turnover and the catabolic fate of the B apoprotein of very low density lipoprotein (VLDL-B) was studied in 15 normal and hyperlipidemic subjects using reinjected autologous VLDL labeled with radioiodine. The specific radioactivity-time curve ofthe B apoprotein in total VLDL (Sf 20-400) was multiexponential but conformed to a two-pool model during the first 48 h of catabolism. The flux was highest in several hypertriglyceridemic subjects. The mass of pool A exceeded the intravascular content of VLDL-B by 30% on average, indicating extravascular metabolism of VLDL. The two-pool model might reflect the input of several populations of particles or heterogeneity of catabolic processes or pools. The flux of B apoprotein was also measured in several subclasses of VLDL, in smailler intermediate density lipoproteins, and in low density lipoproteins (LDL). In three subjects the flux was similar in Sf 60-400 and in Sf 12-60 lipoproteins, suggesting that VLDL was catabolized at least to a particle in the density range Sf 12-60. Subsequent catabolism appeared to proceed by two pathways: in normotriglyceridemiic subjects, B apoprotein flux in the Sf 20-400 and in Sf 12-20 lipoproteins was similar, whereas in hypertriglyceridemic subjects flux through Sf 12-20 accounted for only part of the VLDL-B flux.The flux of low density' lipoprotein B apoprotein (LDL-B), which is believed to be derived from VLDL catabolism, was calculated f'rom the area between the specific activity time curves of' VLDL-B and LDL-B. In subjects with normal plasmla triglyceride concentration, LDL-B flux was froml 91% to 113% of that of VLDL-B; but in three hy'pertriglyceridemic subjects showing high rates of VLDL-B transport, LDL-B flux was only one-third that of VLDL-B. This suggests that

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“…The hepatic uptake of component cholesteryl esters of VLDL is followed by gradual hydrolysis (12), and our results suggest that the B apoprotein is also slowly degraded (Table IV). "I-labeled VLDL apoprotein taken up by rat liver is initially coIncentrated at the cell surface, but gradually appears in the region of secondary lysosomes (23). Therefore, it seems likely that rapid hepatic uptake is followed by gradual enzymatic degradation of both lipid and protein components.…”

Section: Methodsmentioning

confidence: 99%