Amino acid synthesis liver

Your liver is also a site for amino acid synthesis such as Serine, Glycine, Glutamic acid and Glutamine. This means that the liver will hang on to some amino acids for bio-synthesis while passing others onto the general circulation for transportation to other organs and tissue. 

Fig. 20.17. Efflux of intermediates from the TCA cycle. In the liver, TCA cycle intermediates are continuously withdrawn into the pathways of fatty acid synthesis, amino acid synthesis, gluconeogenesis, and heme synthesis. In brain, a-ketoglutarate is converted to glutamate and GABA, both neurotransmitters.

Recently, it has been reported that coumarin and some closely related derivatives administered in vivo stimulated the incorporation of labelled amino acids in the liver [223, 224] the endogenous and poly U-directed microsomal protein synthesis were also increased [225]. The relation of this increased de novo protein synthesis to the induction of drug metabolising enzymes is not clear as coumarin was found to inhibit drug metabolism [66]. However, coumarin brought about a decreased incorporation of amino acids by liver slices in vitro [226]. 

Adding insulin to media in which diaphragms are incubated with labeled amino acid stimulates the incorporation of the amino acid into protein. The injection of insulin to normal rats increases the incorporation of labeled amino acids into liver microsomes, and insulin stimulates the incorporation of [ " Cjglycine and [ " Cjphenylalanine into the protein of liver slices of alloxan-diabetic rats. The stimulation of amino acid incorporation into protein under the effect of insulin is independent of the effect of the hormone on glucose penetration in the cells, since it occurs when glucose is absent from the medium. The effect of insulin on protein synthesis raises the question of insulin s site of action in the sequence of steps that lead to the... 

Stimulation of the synthesis of glucose from amino acids in liver and kidney (the... 

Braunstein believes that aminopherases provide the mechanism for amino acid synthesis and deamination in tissues that contain no general deaminases, and that aminopherases also may participate in the general deamination of the Krebs and Bernheim t3 pe that occurs in kidney and in liver. 

Pyruvate kinase possesses allosteric sites for numerous effectors. It is activated by AMP and fructose-1,6-bisphosphate and inhibited by ATP, acetyl-CoA, and alanine. (Note that alanine is the a-amino acid counterpart of the a-keto acid, pyruvate.) Furthermore, liver pyruvate kinase is regulated by covalent modification. Flormones such as glucagon activate a cAMP-dependent protein kinase, which transfers a phosphoryl group from ATP to the enzyme. The phos-phorylated form of pyruvate kinase is more strongly inhibited by ATP and alanine and has a higher for PEP, so that, in the presence of physiological levels of PEP, the enzyme is inactive. Then PEP is used as a substrate for glucose synthesis in the pathway (to be described in Chapter 23), instead... 

Enzyme preparations from liver or microbial sources were reported to show rather high substrate specificity [76] for the natural phosphorylated acceptor d-(18) but, at much reduced reaction rates, offer a rather broad substrate tolerance for polar, short-chain aldehydes [77-79]. Simple aliphatic or aromatic aldehydes are not converted. Therefore, the aldolase from Escherichia coli has been mutated for improved acceptance of nonphosphorylated and enantiomeric substrates toward facilitated enzymatic syntheses ofboth d- and t-sugars [80,81]. High stereoselectivity of the wild-type enzyme has been utilized in the preparation of compounds (23) / (24) and in a two-step enzymatic synthesis of (22), the N-terminal amino acid portion of nikkomycin antibiotics (Figure 10.12) [82]. 

Insulin also plays a role in fat metabolism. In humans, most fatty acid synthesis takes place in the liver. The mechanism of action of insulin involves directing excess nutrient molecules toward metabolic pathways leading to fat synthesis. These fatty acids are then transported to storage sites, predominantly adipose tissue. Finally, insulin stimulates the uptake of amino acids into cells where they are incorporated into proteins. 

Nutrient homeostasis cell uptake of glucose (especially important in adipose and muscle), amino acids (all cells) and fatty acids stimulation of glycolysis but inhibition of gluconeogenesis (liver), synthesis of glycogen (liver and muscle), triglyceride (liver and adipose) and protein (all cells) ... 

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