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Titolo:
Down-regulation of hepatic lecithin : cholesterol acyltransferase gene expression in chronic renal failure
Autore:
Vaziri, ND; Liang, KH; Parks, JS;
Indirizzi:
Univ Calif Irvine, Dept Med, Div Nephrol & Hypertens, Irvine, CA 92717 USAUniv Calif Irvine Irvine CA USA 92717 l & Hypertens, Irvine, CA 92717 USA Wake Forest Univ, Dept Pathol, Comparat Med Sect, Winston Salem, NC 27109 USA Wake Forest Univ Winston Salem NC USA 27109 , Winston Salem, NC 27109 USA
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 6, volume: 59, anno: 2001,
pagine: 2192 - 2196
SICI:
0085-2538(200106)59:6<2192:DOHL:C>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIGH-DENSITY-LIPOPROTEIN; POLYUNSATURATED FATTY-ACIDS; APOLIPOPROTEIN-A-I; HEMODIALYSIS-PATIENTS; UREMIC PATIENTS; SN-2 POSITION; LIPASE; PLASMA; ABNORMALITIES; RECEPTOR;
Keywords:
high-density lipoprotein; LCAT; lipid disorder; arteriosclerosis; cardiovascular disease; hypertriglyceridemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Vaziri, ND UCI Med Ctr, Div Nephrol & Hypertens, 101 City Dr, Orange, CA 92868 USA UCI Med Ctr 101 City Dr Orange CA USA 92868 range, CA 92868 USA
Citazione:
N.D. Vaziri et al., "Down-regulation of hepatic lecithin : cholesterol acyltransferase gene expression in chronic renal failure", KIDNEY INT, 59(6), 2001, pp. 2192-2196

Abstract

Background. Chronic renal failure (CRF) is associated with premature arteriosclerosis, impaired high-density lipoprotein (HDL) maturation, increased pre-beta HDL (a lipid-poor HDL species), reduced HDL/total cholesterol ratio, hypertriglyceridemia, and depressed lipolytic activity. The latter has been, in part, attributed to elevated pre-beta HDL, which is a potent inhibitor of lipoprotein lipase (LPL). Accumulation of cholesterol in the arterial wall is a critical step in atherogenesis, and HDL-mediated cholesterol removal from peripheral tissues mitigates atherosclerosis. Lecithin:cholesterol acyltransferase (LCAT) is essential for maturation of HDL and cholesterol removal by HDL from peripheral tissues. Earlier studies have revealed depressed plasma LCAT enzymatic activity in patients with CRF. This study was conducted to determine whether impaired LCAT activity can he confirmed in CRF animals and if so whether it is due to down-regulation of hepatic LCAT expression. Methods. Hepatic tissue LCAT mRNA and plasma LCAT enzymatic activity were measured in male Sprague-Dawley rats six weeks after excisional 5/6 nephrectomy or sham operation. Results. Compared with the controls, the CRF group exhibited a significantreduction of hepatic tissue LCAT mRNA abundance. The reduction in hepatic LCAT mRNA was accompanied by a marked reduction of plasma LCAT activity andelevation of serum-free cholesterol in the CRF animals. LCAT activity correlated positively with the HDL/total cholesterol ratio and inversely with free cholesterol and triglyceride concentrations. Conclusions. CRF leads to a marked down-regulation of hepatic LCAT mRNA expression and plasma LCAT activity. This abnormality can impair HDL-mediatedcholesterol uptake from the vascular tissue and contribute to cardiovascular disease. In addition, LCAT deficiency can, in part, account for elevatedserum-free cholesterol, reduced HDL/total cholesterol, and elevated pre-beta HDL in CRF. The latter can, in turn, depress lipolytic activity and hinder triglyceride-rich lipoprotein clearance in CRF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 16:01:59