NUTRITN 430 Lecture Notes - Lecture 14: Glucocorticoid, Catabolism, Oxidative Deamination
30 Jun 2016
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Transamination: transfer of amino group from 1 amino acid to an alpha-keto acid via vitamin b6 (plp-pyridoxal phosphate) to carry the amino group via amino transferases. Ex: alanine + alpha-ketoglutarate pyruvate + glutamate (gpt) (1) Glutamate + oxaloacetate alpha-ketoglutarate + aspartate (got) Ex: glutamate = h2o, nad+ -> nadh => alpha-ketoglutarate + nh3. Nad+ + glutamate akg + nh4+ + nadh. = alanine + nad+ aka + nh4 + nadh. In the liver, transamination is particularly active compared to other tissues also associated with gluconeogenesis. The liver monitors supply of aas to the body and is the primary site for aa degradation. Bcaas go unmonitored because bcaa transferase is very limited in the liver. The transferases that catalyze the transamination are increased when responding to glucocorticoids, similar to enzyme that catalyzes gluconeogenesis. Catabolism of glycogenic aas (such as (1)), contribute to liver glucose level. Urea cycle allows ammonia to be converted to urea and excreted via kidneys.
