Hypercatabolic state

The rate and pattern of amino acid utilization by different tissues change with dietary and physiologic state. Two such states, the postprandial period following a high-protein meal and the hypercatabolic state produced by sepsis or surgical trauma, differ from the postabsorptive state with respect to the availability of amino acids and other fuels and the levels of different hormones in the blood. As a result, the pattern of amino acid utilization is somewhat different. 

In these hypercatabolic states, skeletal muscle protein synthesis decreases, and protein degradation increases. Oxidation of BCAA is increased and glutamine production enhanced. Amino acid uptake is diminished. Cortisol is the major hormonal mediator of these responses, although certain cytokines may also have direct effects on skeletal muscle metabohsm. As occurs during fasting and metabolic acidosis, increased levels of cortisol stimulate ubiquitin-mediated proteolysis, induce the synthesis of glutamine synthetase, and enhance release of amino acids and glutamine from the muscle cells. 

Hypercatabolic states may be accompanied by varying degrees of insulin resistance caused, in part, by the release of counterregulatory hormones into the blood. Thus, patients with diabetes mellitus may require higher levels of exogenous insulin during sepsis. 

This chapter is concerned only with the primary defects in the cellular or humoral immune response. Thus, all hypercatabolic states or those due to exogenous agents, such as irradiation or drugs, are excluded as are im-munodeficient states secondary to malignant processes. The primary immunodeficiencies are categorized in the accompanying tabled... 

Glutamine deficiency occurs in critically ill patients, especially burn patients, as a result of increased protein turnover in the hypercatabolic state (56,57). Low levels of Glutamine on admission are associated with shock and increased hospital mortality and are more common in older persons (58). Glutamine supplementation in ICU patients was reviewed by the Italian Society of Enteral and Parenteral Nutrition (SINPE) (59), which noted that increased plasma glutamine levels were associated with improved outcomes in ICU patients. Other antioxidants such as parenteral selenium are also of interest in ICU patients (60). 

Our data suggest that the zinc-deficient state may have led to hypercatabolism of fat in our subjects. This is suggested by an Increased fat loss and normal absorption of fat during the zinc restriction phase. In experimental animals an Increase in free fatty acids has been observed as a result of zinc deficiency (17). Indeed, more studies are required in human subjects to document Increased fat catabolism due to zinc restriction. 

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