Cachexia as a consequence of a catabolic state (stress metabolism) and cachexia as a consequence of too small food intake (inanition metabolism) have to be distinguished from each other fundamentally. A typical amino acid distribution in plasma, muscle, and liver can be observed in the protein catabolic patient. The glutamine metabolism seemed to be of special interest in the severe catabolic patient (e. g. sepsis). Glutamine is the amino acid with the biggest part of the free amino acid pool. This glutamine pool is reduced in the protein catabolic patient. A connexion seems to exist between the lower muscle glutamine concentration and the prognosis of the patient. The parenteral nutrition can stimulate the protein synthesis, but not suppress the protein hydrolysis. Perhaps catabolic factors as, for instance, interleucine I take part in that. These stimulate the protein hydrolysis over the prostaglandin metabolism.