Nephrology Dialysis Transplantation, Vol 14, Issue 6 1462-1466, Copyright © 1999 by Oxford University Press
N Vaziri, G Deng and K Liang
Background: Chronic renal failure (CRF) is associated
with hypertriglyceridaemia and depressed plasma high-density lipoprotein
(HDL)-cholesterol and apolipoprotein (A-I (Apo A-I) concentrations. Uraemic
hypertriglyceridaemia is due, in part, to lipoprotein lipase and hepatic
lipase deficiencies, which are causally linked to excess parathormone
(PTH). This study was designed to test the hypothesis that depressed plasma
concentration and abnormal composition of HDL in CRF may be due to
dysregulation of hepatic expression of Apo A-I and/or the newly discovered
HDL receptor. Methods: Hepatic Apo A-I and HDL
receptor mRNA abundance (Northern blot), and HDL receptor protein mass
(Western blot) were determined in CRF rats (5/6 nephrectomy),
parathyroidectomized CRF rats (CRF-PTx) and sham-operated controls.
Results: The CRF group exhibited normal hepatic HDL
receptor mRNA and HDL receptor protein abundance coupled with reduced
hepatic Apo A-I mRNA. Hepatic Apo A-I mRNA, HDL receptor mRNA and protein
abundance were not affected by PTx. Conclusions: CRF
results in the down-regulation of hepatic Apo A-I gene expression, which
accounts for the known reduction in plasma Apo A-I concentration. However,
CRF does not affect HDL receptor mRNA or protein expression in this model.
Neither Apo A-I nor HDL receptor expression were modified by PTx in CRF
rats. Key words: cholesterol; hyperlipidaemia; renal
disease; scavenger receptor; triglycerides; uraemia
ORIGINAL ARTICLES
Hepatic HDL receptor, SR-B1 and Apo A-I expression renal failure
Division of Nephrology and Hypertension, Department of Medicine, UCI Medical Centre, 101 The City Drive, Orange, CA 92868, USA; Corresponding author
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