Abstract | OBJECTIVE: METHODS AND RESULTS: We conducted a radiotracer study in LCAT- def (n=2) and normal controls (n=10) and a stable isotope study in one patient and other controls (n=7). LCAT- def LDL was catabolized faster than control LDL in the control subjects as well as in LCAT- def patients. Control LDL was catabolized faster in LCAT- def patients than the controls. The production rate of LDL apolipoprotein B-100 was normal in LCAT- def. The increased LDL apoB-100 catabolism was confirmed by a stable isotope study. LpX was catabolized more slowly in LCAT- def. CONCLUSIONS: The decreased LDL in LCAT- def is attributable to an increased catabolism caused by a rapid catabolism of abnormal LDL and an upregulation of LDL receptor pathway. The decreased catabolism of LpX contributes to its accumulation in LCAT- def.
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Authors | Masato Nishiwaki, Katsunori Ikewaki, Giovanni Bader, Hassan Nazih, Minna Hannuksela, Alan T Remaley, Robert D Shamburek, H Bryan Brewer Jr |
Journal | Arteriosclerosis, thrombosis, and vascular biology
(Arterioscler Thromb Vasc Biol)
Vol. 26
Issue 6
Pg. 1370-5
(Jun 2006)
ISSN: 1524-4636 [Electronic] United States |
PMID | 16543491
(Publication Type: Journal Article)
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Chemical References |
- Apolipoprotein B-100
- Apolipoproteins B
- Lipids
- Lipoprotein-X
- Lipoproteins, LDL
- Radioactive Tracers
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Topics |
- Adult
- Apolipoprotein B-100
- Apolipoproteins B
(biosynthesis, blood)
- Case-Control Studies
- Chromatography, Liquid
- Female
- Humans
- Kinetics
- Lecithin Cholesterol Acyltransferase Deficiency
(blood, metabolism)
- Lipids
(blood)
- Lipoprotein-X
(blood, metabolism)
- Lipoproteins, LDL
(blood, metabolism)
- Male
- Middle Aged
- Radioactive Tracers
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