Role of Factors Derived from Activated Macrophages in Regulation of Muscle Protein Turnover

Abstract

A marked loss of body weight and body protein, and a generalized wasting of skeletal muscle, frequently accompany infection, injury and certain neoplastic diseases (1, 2). These conditions result in a negative nitrogen balance, which may exceed that seen in fasting (2–9). This net nitrogen loss may result from increased degradation of cell protein, reduced rates of protein synthesis, or both (2–9). Skeletal muscle, which comprises a major body protein reserve, would appear to be a primary site for this catabolic response (2–9). Experimental infections, injury or tumours result in a marked loss of muscle mass, and enhancement of protein breakdown in muscle (2, 3, 7, 8). Similarly, in human patients, there is evidence of increased muscle proteolysis and net release of amino aids from this tissue (4, 10). However, the factor(s) initiating muscle catabolism have still to be fully characterized.