Figure 187

Protein catabolism in acute renal failure (ARF). Amino acids are redistributed from muscle tissue to the liver. Hepatic extraction of amino acids from the circulation—hepatic gluconeogenesis, A, and ureagenesis, B, from amino acids all are increased in ARF [12]. The dominant mediator of protein catabolism in ARF is this accel erated hepatic gluconeogenesis, which cannot be suppressed by exogenous substrate infusions (see Fig. 18-15). In the liver, protein synthesis and secretion of acute phase proteins are also stimulated. Circles—livers from acutely uremic rats; squares—livers from sham operated rats. (From Fröhlich [12]; with permission.).

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