Abstract | BACKGROUND: Hereditary analbuminemia is associated with hypercholesterolemia, which has been shown to be primarily caused by increased extrahepatic production of cholesterol. Nagase rats with hereditary analbuminemia (NAR) have been used as a model to dissect the effect of primary hypoalbuminemia from that caused by proteinuria in nephrotic syndrome. The present study was undertaken to explore the effect of hereditary analbuminemia on protein expression of the key factors involved in cholesterol metabolism. METHODS: RESULTS: CONCLUSION:
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Authors | Kaihui Liang, Nosratola D Vaziri |
Journal | Kidney international
(Kidney Int)
Vol. 64
Issue 1
Pg. 192-8
(Jul 2003)
ISSN: 0085-2538 [Print] United States |
PMID | 12787409
(Publication Type: Journal Article)
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Chemical References |
- Carrier Proteins
- Lipoproteins, HDL
- RNA-Binding Proteins
- Receptors, LDL
- Receptors, Lipoprotein
- Serum Albumin
- high density lipoprotein receptors
- high density lipoprotein binding protein
- Hydroxymethylglutaryl CoA Reductases
- Cholesterol 7-alpha-Hydroxylase
- Acyltransferases
- Sterol O-Acyltransferase
- Phosphatidylcholine-Sterol O-Acyltransferase
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Topics |
- Acyltransferases
(metabolism)
- Animals
- Blood Protein Disorders
(enzymology, genetics, metabolism)
- Carrier Proteins
- Cholesterol 7-alpha-Hydroxylase
(metabolism)
- Hydroxymethylglutaryl CoA Reductases
(metabolism)
- Lipoproteins, HDL
- Male
- Phosphatidylcholine-Sterol O-Acyltransferase
(metabolism)
- RNA-Binding Proteins
- Rats
- Rats, Inbred Strains
- Rats, Sprague-Dawley
- Receptors, LDL
(metabolism)
- Receptors, Lipoprotein
(metabolism)
- Serum Albumin
(deficiency)
- Sterol O-Acyltransferase
(blood, metabolism)
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