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Tyrosine liver uptake

An increase in the aromatic amino acids phenylalanine and tyrosine occurs due to the lowered hepatic uptake of enterally released amino acids and their restricted catabolism in the liver. They are also released to a greater extent from the muscles in cases of cirrhosis with catabolism. Furthermore, phenylalanine hydroxylase... [Pg.267]

Early experiments by Bernheim, Felix, Sealock, and their co-workers on oxidation of tyrosine by liver breis showed an uptake of four atoms of oxygen per mole of tyrosine, with the production of one molecule each of carbon dioxide and acetoacetate, but no ammonia (60, 61, 261, 262, 789, 976). Felix and Zorn (261) found alanine to be formed and considered this to arise from a direct splitting of the tyrosine side chain. Although the experiments with man and intact animals already described made it seem very probable that p-hydroxyphenylpyruvic acid and homogentisic acid were normal intermediates in tyrosine metabolism, and although homogentisic acid was known to be readily metabolized by normal liver (e.g., 208, 695, 976) Felix and co-workers (262) considered p-hydroxyphenylpy-ruvic acid and homogentisic acid not to be intermediates in the breakdown of tyrosine by the liver system. [Pg.55]

The plasma concentration of LNAA competes with tryptophan for uptake into the brain. The extent of uptake and net utilization influences levels in blood. Like tryptophan, tyrosine and phenylalanine are mainly metabolized in the liver.199 However, the branched-chain amino acids (BCAA) are taken up and metabolized mainly by skeletal muscle and little by the liver.200 Thus, following a meal, the BCAA rise more in peripheral blood than the other LNAA and other indispensable amino acid levels that are influenced by liver metabolism. The BCAA, therefore, have the dominating effect of the LNAA as a group on brain tryptophan uptake. [Pg.55]

Toluene — Toluene, after intraperitoneal injections or after inhalation, caused a decrease in rat plasma concentrations of tryptophan as well as of tyrosine.54 The mechanism for this is not clear. It may be related to the direct effect of toluene on the liver cell membranes, with a subsequent increase in liver cell uptake of amino acids. [Pg.76]

When occupied, the insulin receptor becomes an active tyrosine kinase enzyme that causes a phosphorylation cascade that ultimately has the opposite effect of the glucagon/cAMP system the enzymes of glycogenolysis are inhibited and the enzymes of glycogenesis are activated. Insulin also increases the rate of glucose uptake into several types of target cells, but not liver or brain cells. [Pg.270]

Recently extracts of acetone powder and homogenates of liver have been obtained which specifically oxidize tyrosine, p-hydroxyphenyl-pyruvic acid, and homogentisic acid to acetoacetic acid. The reaction is aerobic and requires the uptake of 4 atoms of oxygen per molecule for the oxidation of either L-tyrosine or p-hydroxyphenylpyruvic acid to yield 1 molecule of CO2 and 1 of acetoacetic acid oxidation of homogentisic acid to acetoacetate requires the uptake of 2 atoms of oxygen. [Pg.84]


See other pages where Tyrosine liver uptake is mentioned: [Pg.911]    [Pg.530]    [Pg.24]    [Pg.2418]    [Pg.59]    [Pg.174]    [Pg.175]    [Pg.460]    [Pg.766]    [Pg.471]    [Pg.209]    [Pg.520]    [Pg.73]    [Pg.399]    [Pg.424]    [Pg.378]    [Pg.216]    [Pg.128]    [Pg.10]    [Pg.9]   
See also in sourсe #XX -- [ Pg.13 ]




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