There is a close relationship between ammonium and glucose metabolism in liver disease and failure, particularly in cirrhosis after acquired or surgical portasystemic venous shunting. (The term "blood ammonium" is used in referring to ammonia in blood because in excess of 99% of ammonia in the blood is present as ammonium ions.) Many well-documented reports both of elevated blood ammonium levels and of abnormal glucose tolerance curves in advanced cirrhosis1,2 support this statement. The relationship is a very logical one chemically for both the Krebs tricarboxylic acid cycle for carbohydrate metabolism and the Krebs-Henseleit urea cycle for ammonia utilization function in part through use of common intermediates such as oxaloacetate and aspartate (Fig 1). The figure also indicates the three principal known routes for nitrogen fixation into amino acids, purines, nucleic acids, etc, through interrelationship of the two cycles by means of (1) glutamic acid, (2) glutamine, and (3)
Brown H, Brown ME, Covelli VH, McDermott WV. Ammonium and Glucose Metabolism in Liver Failure. JAMA. 1967;201(11):873–874. doi:10.1001/jama.1967.03130110099029
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