Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats |
| |
Authors: | MP Mollica S Iossa S Soboll G Liverini |
| |
Institution: | (1) Department of General and Environmental Physiology, University of Naples 'Federico II', Via Mezzocannone 8, I-80134 Napoli (Italy), Fax + 390812535090, e-mail: susiossa@unina.it, IT;(2) Institute of Physiological Chemistry I, University of Düsseldorf (Germany), DE |
| |
Abstract: | The effect of treatment with acetyl-L-carnitine on hepatic mitochondrial respiration and biosynthetic function in perfused
liver from young (90 days) and old (22-24 months) rats was studied. Rats were given a 1.5% (w/v) solution of acetyl-L-carnitine
in their drinking water for 1 month and oxygen consumption together with the rate of gluconeogenesis, urea synthesis, and
ketogenesis with and without added substrates were measured in perfused liver. Mitochondrial oxygen consumption was also assessed
in liver homogenate and isolated mitochondria to determine the maximal capacity for oxidative phosphorylation. Acetyl-L-carnitine
treatment almost completely restored the age-dependent decline in oxygen consumption, gluconeogenesis, urea synthesis, and
ketogenesis found in perfused liver of old rats to the levels found in young rats. In addition, acetyl-L-carnitine treatment
increased oxygen consumption and biosynthetic function in perfused liver from young rats. After acetyl-L-carnitine treatment,
we found detectable 3-oxoacyl-CoA-transferase activity associated with a consumption of ketone bodies in young and old rats.
Finally, oxygen consumption measured in homogenate and isolated mitochondria did not change with age and acetyl-L-carnitine
treatment. Our results show that in perfused liver, acetyl-L-carnitine treatment slows the age-associated decline in mitochondrial
respiration and biosynthetic function. In addition, treatment of young rats with acetyl-L-carnitine has a stimulating effect
on liver metabolism, probably through an increase in ATP production.
Received 25 October 2000; received after revision 14 December 2000; accepted 11 January 2001 |
| |
Keywords: | : Gluconeogenesis urea synthesis ketogenesis isolated mitochondria ageing |
本文献已被 PubMed SpringerLink 等数据库收录! |
|