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Titolo:
Acquired lecithin-cholesterol acyltransferase deficiency in nephrotic syndrome
Autore:
Vaziri, ND; Liang, K; Parks, JS;
Indirizzi:
Univ Calif Irvine, Dept Med, Div Nephrol, Irvine, CA 92697 USA Univ Calif Irvine Irvine CA USA 92697 , Div Nephrol, Irvine, CA 92697 USA Wake Forest Univ, Bowman Gray Sch Med, Dept Pathol, Winston Salem, NC 27157 USA Wake Forest Univ Winston Salem NC USA 27157 , Winston Salem, NC 27157 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 5, volume: 280, anno: 2001,
pagine: F823 - F828
SICI:
0363-6127(200105)280:5<F823:ALADIN>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
APOLIPOPROTEIN-A-I; POLYUNSATURATED FATTY-ACIDS; PUROMYCIN-INDUCED NEPHROSIS; URINARY-EXCRETION; PLASMA-CONCENTRATION; GENE-EXPRESSION; DOWN-REGULATION; DENSITY-LIPOPROTEINS; ESTER TRANSFER; SN-2 POSITION;
Keywords:
proteinuria; hyperlipidemia; hypercholesterolemia; hypoalbuminemia; hypertriglyceridemia; arteriosclerosis; high-density lipoprotein;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Vaziri, ND UCI Med Ctr, Div Nephrol, 101 City Dr,Bldg 53,Rm 125,Rt 81, Orange, CA 92868 USA UCI Med Ctr 101 City Dr,Bldg 53,Rm 125,Rt 81 Orange CA USA 92868
Citazione:
N.D. Vaziri et al., "Acquired lecithin-cholesterol acyltransferase deficiency in nephrotic syndrome", AM J P-REN, 280(5), 2001, pp. F823-F828

Abstract

Lecithin-cholesterol acetyltransferase (LCAT) is involved in the synthesisof plasma cholesteryl esters and is pivotal in the maturation of plasma high-density lipoprotein (HDL) and conversion of HDL3 to HDL2. In nephrotic syndrome (NS), the ratio of HDL2 to HDL3 is low even though the total concentration of HDL is generally normal. We hypothesize that the reduced HDL2/HDL3 ratio in NS is due to urinary losses of LCAT, leading to plasma LCAT deficiency. To test this hypothesis, Sprague-Dawley rats were randomized to NS(given 130 mg puromycin aminonucleoside on day 1 and 60 mg ip on day 14) or control groups and were studied on day 30. To dissect the effect of proteinuria from hypoalbuminemia, a group of Nagase rats with inherited hypoalbuminemia was included. Hepatic LCAT and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA abundance and plasma and urine LCAT activity were measured. The NS group showed a fourfold rise in serum cholesterol and triglycerides, a fivefold rise in free cholesterol, and a fourfold fall in the HDL-to-total cholesterol ratio. Despite severe hypoalbuminemia, the Nagase rats showed only a mild elevation of serum cholesterol and triglycerides with a normal serum free cholesterol and HDL-to-total cholesterol ratio. The NS group exhibited a normal hepatic LCAT-to-GAPDH mRNA ratio, a marked reduction in plasma LCAT activity, and a significant increase in urinary LCAT excretion. LCAT/GAPDH mRNA and plasma and urine LCAT were normal in Nagase rats. Thus NS led to heavy urinary losses and reduced plasma concentration of LCAT,despite normal hepatic LCAT mRNA abundance. However, hypoalbuminemia, per se, without proteinuria as seen in the Nagase rats had no effect on plasma LCAT or the HDL-to-total cholesterol ratio. Therefore, proteinuria, not hypoalbuminemia, causes LCAT deficiency and a depressed HDL-to-total cholesterol ratio in NS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:24:24