Leucine metabolism in tnf-( and endotoxin treated rats. the
contribution of hepatic tissue..
Holeek, M., L. [grave]eprongl, F. Skopec, C. Andrs, and M. Pecka.
Departments of Physiology, Immunology, Medicine, and Radioisotope
Laboratory, Charles University School of Medicine, Hradec
Kr[beta]lov[theta]; and University Hospital Motol, Prague, Czech
Republic
APStracts 4:0181E, 1997.
The effects of tumor necrosis factor alpha (TNF-(; cachectin) and
lipopolysaccharide of Salmonella enteritidis (LPS; endotoxin) on
leucine metabolism in rats were evaluated in the whole body using
i.v. infusion of L-[1-14C]leucine and in isolated perfused liver
(IPL) using the single pass perfusion technique with (-keto[1
-14C]isocaproate as a tracer for measurement of ketoisocaproic acid
(KIC) oxidation, and the recirculation technique for measurement of
hepatic amino acid exchanges. The data obtained in TNF-( and LPS
groups were compared with those obtained in controls. Both TNF-( and
LPS treatment induced an increase of whole-body leucine turnover,
oxidation and clearance. As the result of a higher increase of
leucine oxidation than of incorporation into the pool of body
proteins, the fractional oxidation of leucine was increased. The
fractional rate of protein synthesis increased significantly in the
spleen (both in TNF-( and LPS rats), in blood plasma, liver, colon,
kidneys and gastrocnemius muscle (in LPS rats) and in lungs (TNF-(
treated rats) while it decreased in the jejunum (LPS rats). In IPL of
TNF-( and LPS treated rats a decrease of KIC oxidation and higher
uptake of branched-chain amino acids (BCAA; valine, leucine, and
isoleucine) were observed when compared with control animals. We
hypothesize that the negative consequences of increased whole-body
proteolysis and of increased oxidation of BCAA induced by TNF-(
and/or LPS are reduced by decreased activity of hepatic branched
-chain ketoacid dehydrogenase that can help resupply BCAA to the body.
Received 18 February 1997; accepted in final form 8 August 1997,
APS Manuscript Number E79-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 27 August 1997